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1
Yan, Rong, Kang Li, Dawei Yuan, Haonan Wang, Wei Chen, Kun Zhu, and Chengxue Dang. "miR-183-5p promotes proliferation and migration in hepatocellular carcinoma by targeting IRS1 and its association with patient survival." International Journal of Biological Markers 35, no. 3 (September 2020): 83–89. http://dx.doi.org/10.1177/1724600820951572.
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Background: MiR-183-5p plays an important role in the pathophysiology of many tumors, while the role of MiR-183-5p in liver cancer is unclear. Methods: In this study, quantitative reverse transcription-polymerase chain reaction and Western blotting were used to detect the expression of miR-183-5p in liver cancer cell lines, liver cancer tissues, and normal tissues adjacent to the cancer, and to explore the mechanism of miR-183-5p regulating liver cancer progression. The in vitro effects of miR-183-5p were evaluated by CCK-8, colony formation test, and wound healing test. Various databases were used to predict the target mRNA of miR-183-5p and verified by luciferase report analysis. In addition, the effects of miR-183-5p and its target gene on the survival of patients with liver cancer were also analyzed. Results: miR-183-5p was highly expressed in hepatocellular carcinoma cells and tissues, and was related to some clinicopathological features. MiR-183-5p can promote the proliferation and migration of liver cancer cells. Using the bioinformatics database, we proved that miR-183-5p is related to the survival of liver cancer patients. Insulin receptor substrate 1 (IRS1) is a target of miR-183-5p, and luciferase analysis confirmed that miR-183-5p combines with the 3′-untranslated region (3′-UTR) of IRS1. Conclusion: The miR-183-5p/IRS1 axis may be a new target for liver cancer research.
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Wu, Chihua, Youlin Tuo, Gang Hu, and Jing Luo. "miR-183-5p Aggravates Breast Cancer Development via Mediation of RGS2." Computational and Mathematical Methods in Medicine 2021 (November 20, 2021): 1–9. http://dx.doi.org/10.1155/2021/9664195.
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This study mainly explores how miR-183-5p pertains to breast cancer (BC) development. Functional assays were employed to test impacts of miR-183-5p in this cancer. Targeting between RGS2 and miR-183-5p was examined with dual-luciferase assay, and how their interaction pertains to cancer progression was further unraveled. miR-183-5p level was noticeably high in cancer tissue/cells. Overexpressing miR-183-5p could remarkably deteriorate cancer progression. The regulatory gene RGS2 levels was markedly low in BC, and two genes we researched were negatively correlated. It was uncovered by rescue assay that miR-183-5p/RGS2 axis mediated tumor-relevant behaviors in BC. Altogether, miR-183-5p aggravates BC development via mediation of RGS2. miR-183-5p supplies a promising target for BC therapy.
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Li, Peiyi, Caifeng Gao, and Zhiyun Chen. "Effect of Bone Marrow Mesenchymal Stem Cells (BMSCs) with High miR-183-5p Expression on Ovarian Cancer Cells by Regulating Signal Transducer and Activator of Transcription 3 (STAT3)." Journal of Biomaterials and Tissue Engineering 12, no. 9 (September 1, 2022): 1692–98. http://dx.doi.org/10.1166/jbt.2022.3093.
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Currently, the treatment for ovarian cancer (OC) is not satisfactory. The microRNAs may have an important function in tumor pathogenesis. miR-183-5p involves in several tumors. However, its effect on OC cells is unclear. The BMSCs could regulate the micro-environment of tumor and participate in tumor procession. In this study, effect of BMSCs with highly-expressed miR-183-5p on OC cells was assessed. The BMSCs with highly-expressed miR-183-5p was established and co-cultivated with OC cell line SKOV3 followed by measuring miR-183-5p level by PCR, STAT3 and ADAM9 expression by western blot. miR-183-5p level in OC cells was reduced and further decreased after co-culture with BMSCs along with enhance cell proliferation and upregulated STAT3 expression (P < 0.05). In addition, miR-183-5p level was increased in BMSCs with highly-expressed miR-183-5p and STAT3 expression was reduced along with restrained cell proliferation (P < 0.05). In conclusion, miR-183-5p in OC cells is downregulated and malignant biological behaviors of OC cells are restrained by BMSCs with highly-expressed miR-183-5p possibly through regulating the expression of STAT3.
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Akbar, Rubab, Kamran Ullah, Tanzil Ur Rahman, Yi Cheng, Hai-Yan Pang, Lu-Yang Jin, Qi-Jing Wang, He-Feng Huang, and Jian-Zhong Sheng. "miR-183-5p regulates uterine receptivity and enhances embryo implantation." Journal of Molecular Endocrinology 64, no. 1 (January 2020): 43–52. http://dx.doi.org/10.1530/jme-19-0184.
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Receptive endometrium is a prerequisite for successful embryo implantation, and it follows that poor endometrial receptivity is a leading cause of implantation failure. miRNAs play important roles as epigenetic regulators of endometrial receptivity and embryo implantation through post-transcriptional modifications. However, the mechanisms of action of many miRNAs are poorly understood. In this study, we investigated the role of the miR-183 family, comprising three miRNAs (miR-183-5p, miR-182-5p, and miR-96-5p) in endometrial receptivity and embryo implantation. The miR-183 family shows estrogen-dependent upregulation in endometrial Ishikawa (IK) cells. The miR-183 family also has a positive role in migration and proliferation of IK cells. Furthermore, JAr spheroid attachment experiments show that attachment rates were significantly decreased after treatment of IK cells with inhibitors for miR-183-5p and miR-182-5p and increased after treatment with miR-183-5p-mimic and miR-96-5p-mimic, respectively. The downstream analysis shows that catenin alpha 2 (CTNNA2) is a potential target gene for miR-183-5p, and this was confirmed in luciferase reporter assays. An in vivo mouse pregnancy model shows that inhibition of miR-183-5p significantly decreases embryo implantation rates and increases CTNNA2 expression. Downregulation of CTNNA2 in endometrial cells by miR-183-5p may be significant in mediating estrogenic effects on endometrial receptivity. In conclusion, miR-183-5p and the CTNNA2 gene may be potential biomarkers for endometrial receptivity and may be useful diagnostic and therapeutic targets for successful embryo implantation.
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Hua, Mingqiang, Qi Feng, Ju Li, Yu Hou, Shuwen Wang, Anli Liu, Jun Peng, and Ming Hou. "Aberrant Expression of MicroRNAs in CD4+ Cells May Contribute to the Imbalance of Th17/Treg Cells in Primary Immune Thrombocytopenia." Blood 132, Supplement 1 (November 29, 2018): 1140. http://dx.doi.org/10.1182/blood-2018-99-115569.
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Abstract Backgrounds:Primary immune thrombocytopenia (ITP) is an acquired autoimmune disease characterized by reduced platelet count and an increased risk of bleeding. The imbalance of Treg/Th17 cells has been demonstrated in ITP, but the mechanism of Th17/Treg cells imbalance is still not clear. In this study, we aimed to investigate whether the expression of helper T (Th) or Treg cell-related microRNAs, such as miR-183-96-182 cluster, miR-17-5p, miR-99a, miR-146-5p, miR-155-5p, miR-181-5p, and miR-326, regulates the ratio of Th17/Treg in CD4+ T cells and could be used to evaluate the clinical implications of ITP patients. Methods: Peripheral blood was obtained from 54 patients with active ITP and 34 healthy controls. Peripheral blood mononuclear cells (PBMCs) were isolated using Ficoll density-gradient centrifugation and the CD4+ cells were separated by immuno-magnetic microbeads selection. Amplification technique of RT-PCR using stem-loop primers was applied to detect the relative expression of microRNAs (miR-17-5p, miR-99a, miR-96-5p, miR-146a-5p, miR-155-5p, miR-181a-5p, miR-182-5p, miR-183-5, miR-326) and U6 was normalized as control for miRNA quantification. The frequencies of Th17 and Treg cells in peripheral blood were analyzed by flow cytometry. The mRNA expression levels of Il-6, Il-10, Il-17, Rorγ-t and Foxp-3 in CD4+ cells were determined by RT-PCR. Platelet autoantibodies specific for GPIIb/IIIaor GPIb/IX were measured using MAIPA method. CD4+ cells were transfected with miRNAs (miR-99a, miR-182-5p, miR-183-5), mimics or inhibitors, which were used to detect the function of miRNAs. Cytokines in culture medium were determined by ELISA. Results: Our results showed that the relative expression of miR-182-5p and miR-183-5p in CD4+ cells was significantly increased in active ITP patients, compared to healthy controls (miR-182-5p, median 9.2678 vs 5.2723, p < 0.05, Fig. 1a; miR-183-5p, median 5.4435 vs 2.009, p < 0.05, Fig. 1b). In addition, the relative expression of miR-99a in ITP patients was lower than that of healthy controls (median 3.4214 vs 7.9648, p < 0.05; Fig. 1c). Moreover, the frequency of Treg cells decreased significantly in ITP patients compared to those in controls (1.89±1.59% vs 4.12±1.42%, p < 0.05; Fig. 2a), and the percentage of Treg cells was positively correlated with the relative expression of miR-99a in ITP patients(r=0.461, p< 0.05; Fig. 2c) and health controls(r=0.729, p< 0.05; Fig. 2d). Though the percentage of Th17 cells increased in ITP patients compared to the health controls (3.51±2.13%vs 1.85±0.63%, p < 0.05; Fig. 2b), there was no correlation between the percentage of Th17 and the relative expression of microRNAs in ITP patients or health controls. Besides, there was no correlation between the expression of mRNAs (Il-10, Il-17, Rorγ-t and Foxp-3) and microRNAs (miR-99a, miRNA-182-5p or miR-183-5p). No significant correlation was found between the microRNAs expression and platelets counts or different autoantibody subsets in ITP patients. The relative expression of other microRNAs (miR-17-5p, miR-96-5p, miR-146a-5p, miR-155-5p, miR-181-5p, miR-326) revealed no difference in CD4+ cells between ITP patients and health controls. Furthermore, the down-regulated expression of miR-183-5p with inhibitors promoted to the differentiation of Th17 cells(Fig. 3a), while up-regulated expression of miR-99a with mimics contributed to Treg cells in CD4+ cells from ITP patients (Fig. 3b). Meanwhile, the IL-17A in culture medium decreased in inhibitor group of miR-183-5p or miR-183-5p. However, miR-182-5p inhibitor had no effect on the differentiation of Th17 cells. Conclusions: Our results show the abnormal expression of microRNAs (miR-99a, miRNA-182-5p and miR-183-5p) in CD4+ cells and the miR-99a was closely correlated with the Treg cells. The aberrant expression of microRNAs may contribute to the imbalance of Th17/Treg cells in the development of ITP patients and potentially constitute a novel therapeutic target. Disclosures No relevant conflicts of interest to declare.
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Pan, Weikang, Ali Wu, Hui Yu, Qiang Yu, Baijun Zheng, Weili Yang, Donghao Tian, Ya Gao, and Peng Li. "NEAT1 Negatively Regulates Cell Proliferation and Migration of Neuroblastoma Cells by miR-183-5p/FOXP1 Via the ERK/AKT Pathway." Cell Transplantation 29 (January 1, 2020): 096368972094360. http://dx.doi.org/10.1177/0963689720943608.
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Neuroblastoma, a malignant tumor of the sympathetic nervous system, is an aggressive extracranial tumor in childhood. Long noncoding RNAs (lncRNAs) have been discovered to play a key role in the eukaryotic regulatory gene network and be involved in a wide variety of biological processes. We observed that the expression of lncRNA nuclear-enriched abundant transcript-1 (NEAT1) was significantly decreased in human neuroblastoma tissues and cell lines, compared with the normal. We observed cell proliferation, migration, and invasion with Cell Counting Kit-8 assay, colony formation assay, and Transwell assay to investigate the effects of NEAT1, miR-183-5p, or FOXP1 on neuroblastoma cells. And we also used StarBase and luciferase reporter gene assay to predict and confirm the interaction of NEAT1, miR-183-5p, and FOXP1 in neuroblastoma cells. First, overexpression of NEAT1 suppressed cell proliferation and played a key role in cell migration and invasion. In addition, NEAT1 was demonstrated to directly interact with miR-183-5p and exerted its antioncogenic role in neuroblastoma by negatively regulating miR-183-5p expression. miR-183-5p suppressed the expression of FOXP1 and regulated cell proliferation and migration by directly targeting FOXP1 mRNA 3′-untranslated region. Moreover, FOXP1 antagonized the effect of miR-183-5p on the phosphorylation of extracellular-regulated kinase/protein kinase B (ERK/AKT), while FOXP1 siRNA increased the reduced phosphorylation of ERK/AKT caused by miR-183-5p inhibitor in neuroblastoma cells. Taken together, these data showed that NEAT1 negatively regulated cell proliferation and migration of neuroblastoma by the miR-183-5p/FOXP1 axis via suppression of the ERK/AKT pathway. Our findings may provide a new target for the study of pathogenesis and treatment of neuroblastoma.
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Kaken, Habaxi, Shanshan Wang, Wei Zhao, Baoerjiang Asihaer, and Li Wang. "P53 Regulates Osteogenic Differentiation Through miR-153-5p/miR-183-5p-X-Linked IAP (XIAP) Signal in Bone Marrow Mesenchymal Stem Cell (BMSC)." Journal of Biomaterials and Tissue Engineering 12, no. 12 (December 1, 2022): 2427–31. http://dx.doi.org/10.1166/jbt.2022.3204.
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This study assessed P53′s role in BMSC osteogenic differentiation. Osteoporosis model was established and P53 expression in the osteogenic differentiation was detected by RT-PCR. BMSC was cultivated and transfected with siRNA followed by measuring presentation of osteogenic differentiation was detected after cells were. The apoptotic condition of osteogenic differentiation was detected through IF method and protein analysis. The relation between P53 and miR-153-5p/miR-183-5p-XIAP signal axis was detected through bioinformatics and luciferase reporter gene assay. P53 expression was significantly increased after osteogenic differentiation was induced. There was a binding site between P53 and miR-153-5p/miR-183-5p-XIAP signal axis. The apoptotic ability of osteoblast was enhanced after inhibition of the expression of P53. In conclusion, P53 develops crucial action on the regulation of BMSC osteogenic differentiation through miR-153-5p/miR-183-5p-XIAP axis.
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Nguyen, Mai Thi, Kyung-Ho Min, and Wan Lee. "MiR-183-5p Induced by Saturated Fatty Acids Hinders Insulin Signaling by Downregulating IRS-1 in Hepatocytes." International Journal of Molecular Sciences 23, no. 6 (March 10, 2022): 2979. http://dx.doi.org/10.3390/ijms23062979.
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Excessive saturated fatty acids (SFA) uptake is known to be a primary cause of obesity, a widely acknowledged risk factor of insulin resistance and type 2 diabetes. Although specific microRNAs (miRNAs) targeting insulin signaling intermediates are dysregulated by SFA, their effects on insulin signaling and sensitivity are largely unknown. Here, we investigated the role of SFA-induced miR-183-5p in the regulation of proximal insulin signaling molecules and the development of hepatic insulin resistance. HepG2 hepatocytes treated with palmitate and the livers of high-fat diet (HFD)-fed mice exhibited impaired insulin signaling resulting from dramatic reductions in the protein expressions of insulin receptor (INSR) and insulin receptor substrate-1 (IRS-1). Differential expression analysis showed the level of miR-183-5p, which tentatively targets the 3′UTR of IRS-1, was significantly elevated in palmitate-treated HepG2 hepatocytes and the livers of HFD-fed mice. Dual-luciferase analysis showed miR-183-5p bound directly to the 3′UTR of IRS-1 and reduced IRS-1 expression at the post-transcriptional stage. Moreover, transfection of HepG2 hepatocytes with miR-183-5p mimic significantly inhibited IRS-1 expression and hindered insulin signaling, consequently inhibiting insulin-stimulated glycogen synthesis. Collectively, this study reveals a novel mechanism whereby miR-183-5p induction by SFA impairs insulin signaling and suggests miR-183-5p plays a crucial role in the pathogenesis of hepatic insulin resistance in the background of obesity.
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Liu, Yanan, LiZhi Feng, Guo Hou, and Lan Yao. "Curcumin Elevates microRNA-183-5p via Cathepsin B-Mediated Phosphatidylinositol 3-Kinase/AKT Pathway to Strengthen Lipopolysaccharide-Stimulated Immune Function of Sepsis Mice." Contrast Media & Molecular Imaging 2022 (July 30, 2022): 1–10. http://dx.doi.org/10.1155/2022/6217234.
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Curcumin (Cur), a natural polyphenol compound, has been testified to modulate innate immune responses and also showed anti-inflammatory properties. Nevertheless, the mechanism was still poorly unknown, especially regarding Cur-modulated microRNAs (miRNAs) under the inflammatory response. CD39+ regulatory T cells (Tregs) were provided with distinct immunosuppressive action and exerted a critical role in the modulation of immune balance in sepsis. Nevertheless, the impact of Cur on the immune function of sepsis mice has not been reported. In this study, the influence of Cur on the inflammatory response and immune function of sepsis mice via augment of miR-183-5p and Cathepsin B (CTSB)-mediated phosphatidylinositol 3-kinase (PI3K)/AKT pathway was explored. Adoption of 20 mg/kg Cur was for gavage. In the meantime, injection of plasmid vectors of interference with miR-183-5p or CTSB was into the tail vein. Intraperitoneal injection of lipopolysaccharide (10 mg/kg) was to stimulate model of sepsis mice. Histopathological changes of sepsis mice were observed. The contents of tumor necrosis factor-α and Interleukin (IL)-1β and IL-6 in serum of mice were examined. Detection of alanine aminotransferase, aspartate aminotransferase (AST), urea nitrogen (BUN), and creatinine in serum of mice was performed. Test of the percentage of CD39+ Tregs in tail venous blood of mice was implemented. Examination of miR-183-5p, CTSB, and PI3K/AKT was performed. The targeting of miR-183-5p and CTSB was detected. Cur was available to ameliorate the histological damage, to reduce the content of inflammatory factors, AST, and BUN, and to decline the percentage of CD39+ Tregs in tail venous blood of sepsis mice. Elevated miR-183-5p or silenced CTSB was available to further enhance the protection of Cur. Cur was available to accelerate miR-183-5p, which negatively modulated CTSB and Cur-mediated PI3K/AKT pathway via the miR-183-5p/CTSB axis to restrain inflammation of sepsis mice and enhance its immune function.
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Hsu, Yung-Ray, Shu-Wen Chang, Yu-Cheng Lin, and Chang-Hao Yang. "Expression of MicroRNAs in the Eyes of Lewis Rats with Experimental Autoimmune Anterior Uveitis." Mediators of Inflammation 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/457835.
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Purpose.This study aimed to determine the dynamic changes of NF-κB-related microRNAs (miRNAs) and cytokines over the course of experimental autoimmune anterior uveitis (EAAU) and elucidate the possible immunopathogenesis.Materials and Methods.Uveitis was induced in Lewis rats using bovine melanin-associated antigen. The inflammatory activity of the anterior chamber was clinically scored, and leukocytes in the aqueous humor were quantified. RNA was extracted from the iris/ciliary bodies and popliteal lymph nodes to reveal the dynamic changes of eight target miRNAs (miR-155-5p, miR-146a-5p, miR-182-5p, miR-183-5p, miR-147b, miR-21-5p, miR-9-3p, and miR-223-3p) and six cytokine mRNAs (IFN-γ, IL-17, IL-12A, IL-1β, IL-6, and IL-10).In situhybridization of miRNA and enzyme-linked immunosorbent assay quantification of cytokines were performed to confirm the results.Results. Disease activity and leukocyte quantification were maximum at day 15 after immunization. The profiling of miRNA revealed downregulation of miR-146a-5p, miR-155-5p, miR-223-3p, and miR-147b and upregulation of miR-182-5p, miR-183-5p, and miR-9-3p. Cytokine analysis revealed IFN-γ, IL-17, IL-12A, IL-1β, and IL-6 overexpression, with IL-10 downregulation.Conclusions.Dynamic changes of miRNAs were observed over the course of EAAU. By initiating NF-κB signaling, the expressions of downstream cytokines and effector cells from the Th17 and Th1 lineages were sequentially activated, contributing to the disease.
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Geng, N., D. Yun, D. Liu, and P. Liu. "AB0053 LncRNA NUTM2A-AS1 ALLEVIATED OSTEOARTHRITIS BY REGULATING miR-183-5p/TGFA PATHWAY." Annals of the Rheumatic Diseases 81, Suppl 1 (May 23, 2022): 1161.2–1161. http://dx.doi.org/10.1136/annrheumdis-2022-eular.4384.
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BackgroundOsteoarthritis(OA) is a common comorbidity in the elderly, characterized by articular cartilage degeneration, hyperosteogeny and synovitis. Long non-coding RNAs (LncRNAs) have been shown to be involved in several human diseases, including OA. However, the effect of NUTM2A-AS1 on chondrocytes remains unknown.ObjectivesThe purpose of this study was to evaluate the role of LncRNA NUTM2A-AS1 in OA pathological changes in vitro.MethodsChondrocyte cells were treated for 24 hours to mimic OA pathological conditions. The experimental center used chondrocytes with interleukin-1 beta (IL-1β) Intervention to simulate the pathological state of OA.The expression levels of LncRNA NUTM2A-AS1, miR-183-5p and TGFA mRNA were detected by quantitative real-time PCR (qRT-PCR), along with CCK-8 to determine cell viability. Inflammatory response was assessed by determining the release of pro-inflammatory factors such as TNF-α and IL-6 using ELISA kits. Cell apoptosis was examined by flow cytometry assay. The binding relationship between miR-183-5p and LncRNA NUTM2A-AS1 or TGFA was confirmed by dual-luciferase reporter assay.ResultsIL-1β induced chondrocytes to express LncRNA NUTM2A-AS1 and TGFA, and the miR-183-5p expression was decreased in IL-1β-treated cells. Low expression of LncRNA NUTM2A-AS1 or TGFA mitigated IL-1β-caused chondrocyte viability reduction and apoptosis promotion. miR-183-5p overexpression alleviated IL-1β-mediated chondrocyte apoptosis and inflammatory injury via decreasing TGFA expression. In addition, our work revealed that miR-183-5p is a target of LncRNA NUTM2A-AS1. Rescue experiments showed that TGFA overexpression could reverse the effects of low expression of LncRNA NUTM2A-AS1 on the pathological changes in IL-1β-induced chondrocytes.ConclusionLow expression of LncRNA NUTM2A-AS1 significantly mitigated the chondrocytes damage induced by IL-1β through regulating miR-183-5p/TGFA axis, which might be an important target to regulate the promotion of OA.References[1]Kong H, Sun ML, Zhang XA, Wang XQ. Crosstalk Among circRNA/lncRNA, miRNA, and mRNA in Osteoarthritis[J]. Front Cell Dev Biol, 2021, 9:77437Disclosure of InterestsNone declared
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Patterson, E., R. Webb, A. Weisbrod, B. Bian, M. He, L. Zhang, A. K. Holloway, et al. "The microRNA expression changes associated with malignancy and SDHB mutation in pheochromocytoma." Endocrine-Related Cancer 19, no. 2 (January 12, 2012): 157–66. http://dx.doi.org/10.1530/erc-11-0308.
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Currently, the diagnosis of malignant pheochromocytoma can only be made when there is clinical evidence of metastasis or extensive local invasion. Thus, there is a need for new diagnostic marker(s) to identify tumors with malignant potential. The purpose of this study was to identify microRNAs (miRNAs) that are differentially expressed between benign and malignant pheochromocytomas and assess their diagnostic accuracy. Toward this aim, we analyzed miRNA expression in benign and malignant pheochromocytoma tumor samples using whole genome microarray profiling. Microarray analysis identified eight miRNAs that were significantly differentially expressed between benign and malignant pheochromocytomas. We measured a subset of these miRNAs directly by RT-PCR and found that miR-483-5p, miR-183, and miR-101 had significantly higher expression in malignant tumors as compared to their benign counterparts. Area under the receiver operating curve (AUC) analysis indicated that miR-483-5p, miR-101, and miR-183 could be useful diagnostic markers for distinguishing malignant from benign pheochromocytomas. In addition, these miRNAs could be detected in pheochromocytoma patient serum. Overall our data suggest that misexpression of miR-483-5p, miR-101, and miR-183 is associated with malignant pheochromocytoma.
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Yamano, Tomoki, Shuji Kubo, Emiko Sonoda, Tomoko Kominato, Kei Kimura, Michiko Yasuhara, Kozo Kataoka, et al. "Assessment of circulating microRNA specific for patients with familial adenomatous polyposis." PLOS ONE 16, no. 5 (May 4, 2021): e0250072. http://dx.doi.org/10.1371/journal.pone.0250072.
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Circulating microRNAs (miRNAs) are considered promising biomarkers for diagnosis, prognosis, and treatment efficacy of diseases. However, usefulness of circulating miRNAs as biomarkers for hereditary gastrointestinal diseases have not been confirmed yet. We explored circulating miRNAs specific for patients with familial adenomatous polyposis (FAP) as a representative hereditary gastrointestinal disease. Next-generation sequencing (NGS) indicated that plasma miR-143-3p, miR-183-5p, and miR-885-5p were candidate biomarkers for five FAP patients compared to three healthy donors due to moderate copy number and significant difference. MiR-16-5p was considered as an internal control due to minimum difference in expression across FAP patients and healthy donors. Validation studies by real-time PCR showed that mean ratios of maximum expression and minimum expression were 2.2 for miR-143-3p/miR-16-5p, 3.4 for miR-143-3p/miR-103a-3p, 5.1 for miR-183-5p/miR-16-5p, and 4.9 for miR-885-5p/miR-16-5p by using the samples collected at different time points of eight FAP patients. MiR-143-3p/16-5p was further assessed using specimens from 16 FAP patients and 7 healthy donors. MiR-143-3p was upregulated in FAP patients compared to healthy donors (P = 0.04), but not significantly influenced by clinicopathological features. However, miR-143-3p expression in colonic tumors was rare for upregulation, although there was a significant difference by existence of desmoid tumors. MiR-143-3p transfection significantly inhibited colorectal cancer cell proliferation compared to control microRNA transfection. Our data suggested regulation of miR-143-3p expression differed by samples (plasma or colonic tumors) in most FAP patients. Upregulation of plasma miR-143-3p expression may be helpful for diagnosis of FAP, although suppressive effect on tumorigenesis seemed insufficient in FAP patients.
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Qin, Shijie, Xuejia Shi, Canbiao Wang, Ping Jin, and Fei Ma. "Transcription Factor and miRNA Interplays Can Manifest the Survival of ccRCC Patients." Cancers 11, no. 11 (October 28, 2019): 1668. http://dx.doi.org/10.3390/cancers11111668.
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Clear cell renal cell carcinoma (ccRCC) still remains a higher mortality rate in worldwide. Obtaining promising biomakers is very crucial for improving the diagnosis and prognosis of ccRCC patients. Herein, we firstly identified eight potentially prognostic miRNAs (hsa-miR-144-5p, hsa-miR-223-3p, hsa-miR-365b-3p, hsa-miR-3613-5p, hsa-miR-9-5p, hsa-miR-183-5p, hsa-miR-335-3p, hsa-miR-1269a). Secondly, we found that a signature containing these eight miRNAs showed obviously superior to a single miRNA in the prognostic effect and credibility for predicting the survival of ccRCC patients. Thirdly, we discovered that twenty-two transcription factors (TFs) interact with these eight miRNAs, and a signature combining nine TFs (TFAP2A, KLF5, IRF1, RUNX1, RARA, GATA3, IKZF1, POU2F2, and FOXM1) could promote the prognosis of ccRCC patients. Finally, we further identified eleven genes (hsa-miR-365b-3p, hsa-miR-223-3p, hsa-miR-1269a, hsa-miR-144-5p, hsa-miR-183-5p, hsa-miR-335-3p, TFAP2A, KLF5, IRF1, MYC, IKZF1) that could combine as a signature to improve the prognosis effect of ccRCC patients, which distinctly outperformed the eight-miRNA signature and the nine-TF signature. Overall, we identified several new prognosis factors for ccRCC, and revealed a potential mechanism that TFs and miRNAs interplay cooperatively or oppositely regulate a certain number of tumor suppressors, driver genes, and oncogenes to facilitate the survival of ccRCC patients.
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Zhou, Shaolan, Jing Zhang, Pengfei Luan, Zhanbing Ma, Jie Dang, Hong Zhu, Qian Ma, Yanfeng Wang, and Zhenghao Huo. "miR-183-5p Is a Potential Molecular Marker of Systemic Lupus Erythematosus." Journal of Immunology Research 2021 (May 6, 2021): 1–11. http://dx.doi.org/10.1155/2021/5547635.
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Objective. To investigate microRNA (miRNA) expression profiles in individuals with systemic lupus erythematosus (SLE) and identify the valuable miRNA biomarkers in diagnosing and monitoring SLE. Methods. Next-generation sequencing (NGS) was performed to assess miRNA amounts in peripheral blood mononuclear cells (PBMCs) from four SLE cases and four healthy controls. Quantitative polymerase chain reaction (qPCR) was carried out for validating candidate miRNAs in 32 SLE cases and 32 healthy controls. In addition, receiver operating characteristic (ROC) curve analysis was completed to evaluate diagnostic performance. Finally, the associations of candidate miRNAs with various characteristics of SLE were analyzed. Results. A total of 157 miRNAs were upregulated, and 110 miRNAs were downregulated in PBMCs from SLE cases in comparison to healthy controls, of which the increase of miR-183-5p and decrease of miR-374b-3p were validated by qPCR and both showed good diagnostic performance for SLE diagnosis. Besides, miR-183-5p expression levels displayed a positive association with SLE disease activity index (SLEDAI) and anti-dsDNA antibody amounts. Conclusion. Our data indicated that miR-183-5p is a promising biomarker of SLE.
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Zhang, Bao-Le, Fu-Lu Dong, Ting-Wen Guo, Xiao-He Gu, Lin-Yan Huang, and Dian-Shuai Gao. "MiRNAs Mediate GDNF-Induced Proliferation and Migration of Glioma Cells." Cellular Physiology and Biochemistry 44, no. 5 (2017): 1923–38. http://dx.doi.org/10.1159/000485883.
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Background/Aims: Glial cell line-derived neurotrophic factor (GDNF) is an important factor promoting invasive glioma growth. This study was performed to reveal a unique mechanism of glioma cell proliferation and migration. Methods: Human U251 glioma cells were used to screen the optimal GDNF concentration and treatment time to stimulate proliferation and migration. MicroRNA (MiRNA) expression profiles were detected by microarray and confirmed by real-time polymerase chain reaction (PCR). The target genes of differentially expressed miRNAs were predicted by miRWalk, and those targeted by multiple miRNAs were screened with Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. A regulatory miRNA network was constructed using ingenuity pathway analysis (IPA). Target gene expression of differentially expressed miRNAs was examined by real-time PCR or mRNA microarray. Results: The results show that 50 ng/mL GDNF for 24 h significantly promotes U251 glioma cell proliferation and migration (P < 0.05). Seven miRNAs (hsa-miR-194-5p, hsa-miR-152-3p, hsa-miR-205-5p, hsa-miR-629-5p, hsa-miR-3609, hsa-miR-183-5p, and hsa-miR-487b-3p) were significantly up-regulated after GDNF treatment (P < 0.05). These miRNAs are primarily involved in signal transduction, cell adhesion and cell cycle through mitogen-activated protein kinase (MAPK) signaling, focal adhesion and glioma signal pathways. Five of these miRNAs (hsa-miR-194-5p, hsa-miR-152-3p, hsa-miR-205-5p, hsa-miR-183-5p, and hsa-miR-487b-3p) co-regulate TP53 and Akt. mRNA expression levels of four genes co-targeted by two or more up-regulated miRNAs were significantly decreased after GDNF treatment (P < 0.05). Conclusion: GDNF treatment of U251 glioma cells significantly increased the expression of seven miRNAs involved in cell adhesion and the cell cycle.
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Petric, Rok, Barbara Gazic, Katja Goricar, Vita Dolzan, Radan Dzodic, and Nikola Besic. "Expression of miRNA and Occurrence of Distant Metastases in Patients with Hürthle Cell Carcinoma." International Journal of Endocrinology 2016 (2016): 1–6. http://dx.doi.org/10.1155/2016/8945247.
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Background. Hürthle cell thyroid carcinoma (HCTC) is a rare type of thyroid carcinoma. In the present study, we investigated whether the expression of miRNAs of interest is associated with the occurrence of metastases in patients with HCTC.Materials and Methods. In 39 patients with HCTC (22 with nonmetastatic and 17 with regional or distant metastatic disease), the expression levels of six miRNAs (miR-138, miR-183, miR-221, miR-222, miR-768-3p, and miR-885-5p) and U6 snRNA as endogenous control were determined in FFPE samples of primary tumor and normal thyroid tissue using TaqMan miRNA assays.Results. In patients with HCTC, miR-138 and miR-768-3p were downregulated in tumor samples compared to normal tissue (p=0.013andp=0.010, resp.). These two miRNAs were also significantly downregulated in tumor samples of patients with metastatic disease (p=0.030andp=0.048, resp.) but not in patients with nonmetastatic disease (p=0.249andp=0.101, resp.). In patients with nonmetastatic disease, miR-221 and miR-885-5p were slightly, albeit significantly, upregulated in tumorous compared to normal tissue (p=0.042andp=0.027, resp.).Conclusion. Expression of miRNA (miR-183, miR-221, and miR-885-5p) in tumor tissue is associated with the occurrence of distant metastases in patients with HCTC.
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Ambrozkiewicz, Filip, Jakub Karczmarski, Maria Kulecka, Agnieszka Paziewska, Magdalena Cybulska, Michal Szymanski, Jakub Dobruch, Artur Antoniewicz, Michal Mikula, and Jerzy Ostrowski. "Challenges in Cancer Biomarker Discovery Exemplified by the Identification of Diagnostic MicroRNAs in Prostate Tissues." BioMed Research International 2020 (May 6, 2020): 1–4. http://dx.doi.org/10.1155/2020/9086829.
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Identification and clinical translation of routinely tested biomarkers require a complex and multistep workflow. Here, we described a confirmatory process estimating the utility of previously identified candidate tissue miRNAs for diagnosis of prostate cancer (PCa). RNA was isolated from formalin-fixed paraffin-embedded (FFPE) prostate tissue surgically resected from 44 patients with PCa and 24 patients with benign prostate hyperplasia (BPH). Of the 92 RNA samples obtained, 68 represented 42 malignant (PCa) areas and 26 represented nonmalignant (PCa 0%) areas of the prostate tissue sections. The levels of miR-32-5p, miR-183-5p, miR-141-5p, miR-187-3p, miR-375, miR-663b, miR-615-3p, miR-205-5p, miR-221-3p, and miR-222-3p were evaluated using Exiqon chemistry. Five (miR-32-5p, miR-141-5p, miR-187-3p, miR-375, and miR-615-3p), one (miR-32-5p), and two (miR-32-5p and miR-141-5p) miRNAs discriminated between BPH and areas of cancer-bearing prostate tissue harboring different numbers of cancer cells (PCa 15–70%, PCa 2–10%, and PCA 0%, respectively), with an area under the receiver operating characteristics curve (AUC-ROC) > 0.9. Only miRNA 32-5p discriminated BPH specimens from sections of cancer-bearing prostate tissue with a low percentage, a high percentage, or no dysplastic cells. miR-32-5p could be considered as potential diagnostic biomarker discriminating BPH from noncancerous areas within cancer-bearing prostate tissue. However, further clinical studies are warranted to confirm its diagnostic utility.
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Roser, Anna-Elisa, Lucas Caldi Gomes, Rashi Halder, Gaurav Jain, Fabian Maass, Lars Tönges, Lars Tatenhorst, Mathias Bähr, André Fischer, and Paul Lingor. "miR-182-5p and miR-183-5p Act as GDNF Mimics in Dopaminergic Midbrain Neurons." Molecular Therapy - Nucleic Acids 11 (June 2018): 9–22. http://dx.doi.org/10.1016/j.omtn.2018.01.005.
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Eminaga, Okyaz, Fabian Woetzel, Jochen Fries, Susanne Neiss, Michaela Heitmann, Udo Engelmann, Axel Heidenreich, and Ute Warnecke-Eberz. "miRNA expression profiles in high-grade prostatic intraepithelial neoplasia." Journal of Clinical Oncology 34, no. 2_suppl (January 10, 2016): 45. http://dx.doi.org/10.1200/jco.2016.34.2_suppl.45.
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45 Background: High-grade prostatic intraepithelial neoplasia (HGPIN) is widely believed to be a precursor of prostate cancer (PCa). However, little is known about the expression of miRNAs variations in HGPIN compared to normal tissues and PCa. Methods: The expression data of 1054 miRNAs from TCGA were applied to identify relevant miRNAs associated with tumor progression (i.e., miR-98-5p, miR-183-5p, 345-5p, miR-143 miR-210-3p and miR-378-3p). miRNA were isolated by miRNeasy FFPE kit (Qiagen, Hilden, Germany) from paraffin-embedded tissues (FFPE) of prostate specimens with PCa, HGPIN and normal tissues. Early-stage PCa was defined as PCa with pT2 tumor stage, Gleason score <=7a (3+4) and PSA level <10 ng/ml. Quantitative miRNA expression data were acquired and analyzed using a real-time TaqMan-based PCR with the ABI Prism 7900HT (Life Technologies, Darmstadt, Germany). ANOVA analysis were performed to evaluate the expression of miRNAs between HGPIN, Normal and PCa tissues. All statistical analysis was performed using SPSS (IBM, Armonk, USA). P values were adjusted using the false discovery rate for multiple comparisons. The small nuclear U6 RNA was used as an endogenous control. Results: The expression of miR-143-3p, miR-210-3p and miR-345-5p and miR-98-5-p were varied between normal tissue, HGPIN and early-stage PCa. Interestingly, decrease in expression of miR-143.-3p, miR-98-5p and miR-210-3p was associated with tumor development (Normal tissues > HGPIN > early-stage PCa) (FDR<0.001). Furthermore, overexpression of miR-345-5p was observed in normal tissues compared to HGPIN and early-stage PCa, which both showed similar expression level of miR-345-5p. No significant differences in expression of miR-375, miR-183-5p and miR-378-3p were observed between HGPIN and PCa. These miRNAs were interacted with genes related to HIF-1 signaling pathway, p53 signaling pathway, androgen receptor signaling pathway, intrinsic apoptotic signaling pathway, RNA transcription, homologous recombination and non-homologous end-joining. Conclusions: HGPIN shows an altered expression of miRNAs interact with genes related to hypoxia, androgen receptor signaling pathway, cell cycle and epigenetic regulation.
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Visani, Michela, Gianluca Marucci, Dario de Biase, Felice Giangaspero, Francesca Romana Buttarelli, Alba Ariela Brandes, Enrico Franceschi, et al. "miR-196B-5P and miR-200B-3P Are Differentially Expressed in Medulloblastomas of Adults and Children." Diagnostics 10, no. 5 (April 29, 2020): 265. http://dx.doi.org/10.3390/diagnostics10050265.
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Medulloblastoma is a highly aggressive brain tumor that typically affects children, while in adults it represents ~1% of all brain tumors. Little is known about microRNA expression profile of the rare adult medulloblastoma. The main aim of this study was to identify peculiar differences in microRNA expression between childhood and adult medulloblastoma. Medulloblastomas were profiled for microRNA expression using the Exiqon Human miRNome panel (I + II) analyzing 752 microRNAs in a training set of six adult and six childhood cases. Then, the most differentially expressed microRNAs were validated in a total of 21 adult and 19 childhood cases. Eight microRNAs (miR-196b-5p, miR-183-5p, miR-200b-3p, miR-196a-5p, miR-193a-3p, miR-29c-3p, miR-33b-5p, and miR-200a-3p) were differentially expressed in medulloblastoma of adults and children. Analysis of the validation set confirmed that miR-196b-5p and miR-200b-3p were significantly overexpressed in medulloblastoma of adults as compared with those of children. We followed an in silico approach to investigate direct targets and the pathways involved for the two microRNAs (miR-196b and miR-200b) differently expressed between adult and childhood medulloblastoma. Adult and childhood medulloblastoma have different miRNA expression profiles. In particular, the differential dysregulation of miR-196b-5p and miR-200b-3p characterizes the miRNA profile of adult medulloblastoma and suggests potential targets for novel diagnostic, prognostic, or therapeutic strategies.
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Tomeva, Elena, Ulrike D. B. Krammer, Olivier J. Switzeny, Alexander G. Haslberger, and Berit Hippe. "Sex-Specific miRNA Differences in Liquid Biopsies from Subjects with Solid Tumors and Healthy Controls." Epigenomes 7, no. 1 (January 10, 2023): 2. http://dx.doi.org/10.3390/epigenomes7010002.
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Dysregulation of epigenetic mechanisms has been recognized to play a crucial role in cancer development, but these mechanisms vary between sexes. Therefore, we focused on sex-specific differences in the context of cancer-based data from a recent study. A total of 12 cell-free DNA methylation targets in CpG-rich promoter regions and 48 miRNAs were analyzed by qPCR in plasma samples from 8 female and 7 male healthy controls as well as 48 female and 80 male subjects with solid tumors of the bladder, brain, colorectal region (CRC), lung, stomach, pancreas, and liver. Due to the small sample size in some groups and/or the non-balanced distribution of men and women, sex-specific differences were evaluated statistically only in healthy subjects, CRC, stomach or pancreas cancer patients, and all cancer subjects combined (n female/male—8/7, 14/14, 8/15, 6/6, 48/80, respectively). Several miRNAs with opposing expressions between the sexes were observed for healthy subjects (miR-17-5p, miR-26b-5p); CRC patients (miR-186-5p, miR-22-3p, miR-22-5p, miR-25-3p, miR-92a-3p, miR-16-5p); stomach cancer patients (miR-133a-3p, miR-22-5p); and all cancer patients combined (miR-126-3p, miR-21-5p, miR-92a-3p, miR-183-5p). Moreover, sex-specific correlations that were dependent on cancer stage were observed in women (miR-27a-3p) and men (miR-17-5p, miR-20a-5p). Our results indicate the complex and distinct role of epigenetic regulation, particularly miRNAs, depending not only on the health status but also on the sex of the patient. The same miRNAs could have diverse effects in different tissues and opposing effects between the biological sexes, which should be considered in biomarker research.
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Lin, Min-Ying, Yu-Chan Chang, Shan-Ying Wang, Muh-Hwa Yang, Chih-Hsien Chang, Michael Hsiao, Richard N. Kitsis, and Yi-Jang Lee. "OncomiR miR-182-5p Enhances Radiosensitivity by Inhibiting the Radiation-Induced Antioxidant Effect through SESN2 in Head and Neck Cancer." Antioxidants 10, no. 11 (November 14, 2021): 1808. http://dx.doi.org/10.3390/antiox10111808.
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Radiotherapy is routinely used for the treatment of head and neck squamous cell carcinoma (HNSCC). However, the therapeutic efficacy is usually reduced by acquired radioresistance and locoregional recurrence. In this study, The Cancer Genome Atlas (TCGA) analysis showed that radiotherapy upregulated the miR-182/96/183 cluster and that miR-182 was the most significantly upregulated. Overexpression of miR-182-5p enhanced the radiosensitivity of HNSCC cells by increasing intracellular reactive oxygen species (ROS) levels, suggesting that expression of the miR-182 family is beneficial for radiotherapy. By intersecting the gene targeting results from three microRNA target prediction databases, we noticed that sestrin2 (SESN2), a molecule resistant to oxidative stress, was involved in 91 genes predicted in all three databases to be directly recognized by miR-182-5p. Knockdown of SESN2 enhanced radiation-induced ROS and cytotoxicity in HNSCC cells. In addition, the radiation-induced expression of SESN2 was repressed by overexpression of miR-182-5p. Reciprocal expression of the miR-182-5p and SESN2 genes was also analyzed in the TCGA database, and a high expression of miR-182-5p combined with a low expression of SESN2 was associated with a better survival rate in patients receiving radiotherapy. Taken together, the current data suggest that miR-182-5p may regulate radiation-induced antioxidant effects and mediate the efficacy of radiotherapy.
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Shang, Jin, Wei-Min Chen, Zhi-Hong Wang, Tian-Nan Wei, Zhi-Zhong Chen, and Wen-Bing Wu. "CircPAN3 mediates drug resistance in acute myeloid leukemia through the miR-153-5p/miR-183-5p–XIAP axis." Experimental Hematology 70 (February 2019): 42–54. http://dx.doi.org/10.1016/j.exphem.2018.10.011.
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Dettmer, Matthias S., Aurel Perren, Holger Moch, Paul Komminoth, Yuri E. Nikiforov, and Marina N. Nikiforova. "MicroRNA profile of poorly differentiated thyroid carcinomas: new diagnostic and prognostic insights." Journal of Molecular Endocrinology 52, no. 2 (January 17, 2014): 181–89. http://dx.doi.org/10.1530/jme-13-0266.
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The diagnosis of conventional and oncocytic poorly differentiated (oPD) thyroid carcinomas is difficult. The aim of this study is to characterise their largely unknown miRNA expression profile and to compare it with well-differentiated thyroid tumours, as well as to identify miRNAs which could potentially serve as diagnostic and prognostic markers. A total of 14 poorly differentiated (PD), 13 oPD, 72 well-differentiated thyroid carcinomas and eight normal thyroid specimens were studied for the expression of 768 miRNAs using PCR-Microarrays. MiRNA expression was different between PD and oPD thyroid carcinomas, demonstrating individual clusters on the clustering analysis. Both tumour types showed upregulation of miR-125a-5p, -15a-3p, -182, -183-3p, -222, -222-5p, and downregulation of miR-130b, -139-5p, -150, -193a-5p, -219-5p, -23b, -451, -455-3p and of miR-886-3p as compared with normal thyroid tissue. In addition, the oPD thyroid carcinomas demonstrated upregulation of miR-221 and miR-885-5p. The difference in expression was also observed between miRNA expression in PD and well-differentiated tumours. The CHAID algorithm allowed the separation of PD from well-differentiated thyroid carcinomas with 73–79% accuracy using miR-23b and miR-150 as a separator. Kaplan–Meier and multivariate analysis showed a significant association with tumour relapses (for miR-23b) and with tumour-specific death (for miR-150) in PD and oPD thyroid carcinomas. MiRNA expression is different in conventional and oPD thyroid carcinomas in comparison with well-differentiated thyroid cancers and can be used for discrimination between these tumour types. The newly identified deregulated miRNAs (miR-150, miR-23b) bear the potential to be used in a clinical setting, delivering prognostic and diagnostic informations.
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Cao, Jia-Min, Shi-Ying Hou, Xin Qi, and Wei Xiong. "Epigenetics effect on pathogenesis of thyroid-associated ophthalmopathy." International Journal of Ophthalmology 14, no. 9 (September 18, 2021): 1441–48. http://dx.doi.org/10.18240/ijo.2021.09.22.
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Thyroid-associated ophthalmopathy (TAO) is an autoimmune disease. Recent studies have found the aberrant epigenetics in TAO, including DNA methylation, non-coding RNAs, and histone modification. Many genes have an aberrant level of methylation in TAO. For example, higher levels are found in CD14, MBP, ANGLE1, LYAR and lower levels in DRD4 and BOLL. Non-coding RNAs are involved in the immune response (miR-146a, miR-155, miR-96, miR-183), fibrosis regulation (miR-146a, miR-21, miR-29), adipogenesis (miR-27) and are thought to play roles in TAO. MicroRNA is also related to the clinical activity score (miR-Let7d-5p) and may be a predictor of glucocorticoid therapy (miR-224-5p). The quantities of H4 in TAO are increased compared with euthyroid control subjects, and the role of histone modifications in Graves’ disease may lead to better understanding of its role in TAO. More studies are needed to explain the role of epigenetics in TAO and provide potential therapeutic strategies.
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Souza, Marilesia Ferreira, Ilce Mara Syllos Cólus, Aline Simoneti Fonseca, Valquíria Casanova Antunes, Deepak Kumar, and Luciane Regina Cavalli. "MiR-182-5p Modulates Prostate Cancer Aggressive Phenotypes by Targeting EMT Associated Pathways." Biomolecules 12, no. 2 (January 22, 2022): 187. http://dx.doi.org/10.3390/biom12020187.
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Prostate cancer (PCa) is a clinically heterogeneous disease, where deregulation of epigenetic events, such as miRNA expression alterations, are determinants for its development and progression. MiR-182-5p, a member of the miR-183 family, when overexpressed has been associated with PCa tumor progression and decreased patients’ survival rates. In this study, we determined the regulatory role of miR-182-5p in modulating aggressive tumor phenotypes in androgen-refractory PCa cell lines (PC3 and DU-145). The transient transfection of the cell lines with miR-182-5p inhibitor and mimic systems, significantly affected cell proliferation, adhesion, migration, and the viability of the cells to the chemotherapeutic agents, docetaxel, and abiraterone. It also affected the protein expression levels of the tumor progression marker pAKT. These changes, however, were differentially observed in the cell lines studied. A comprehensive biological and functional enrichment analysis and miRNA/mRNA interaction revealed its strong involvement in the epithelial-mesenchymal transition (EMT) process; expression analysis of EMT markers in the PCa transfected cells directly or indirectly modulated the analyzed tumor phenotypes. In conclusion, miR-182-5p differentially impacts tumorigenesis in androgen-refractory PCa cells, in a compatible oncomiR mode of action by targeting EMT-associated pathways.
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Oliveira-Rizzo, Carolina, María Carolina Ottati, Rafael Sebastián Fort, Santiago Chavez, Juan Manuel Trinidad, Andrés DiPaolo, Beatriz Garat, José Roberto Sotelo-Silveira, and María Ana Duhagon. "Hsa-miR-183-5p Modulates Cell Adhesion by Repression of ITGB1 Expression in Prostate Cancer." Non-Coding RNA 8, no. 1 (January 18, 2022): 11. http://dx.doi.org/10.3390/ncrna8010011.
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Prostate cancer is a major health problem worldwide. MiR-183 is an oncomiR and a candidate biomarker in prostate cancer, affecting various pathways responsible for disease initiation and progression. We sought to discover the most relevant processes controlled by miR-183 through an unbiased transcriptomic approach using prostate cell lines and patient tissues to identify miR-183 responsive genes and pathways. Gain of function experiments, reporter gene assays, and transcript and protein measurements were conducted to validate predicted functional effects and protein mediators. A total of 135 candidate miR-183 target genes overrepresenting cell adhesion terms were inferred from the integrated transcriptomic analysis. Cell attachment, spreading assays and focal adhesion quantification of miR-183-overexpressing cells confirmed the predicted reduction in cell adhesion. ITGB1 was validated as a major target of repression by miR-183 as well as a mediator of cell adhesion in response to miR-183. The reporter gene assay and PAR-CLIP read mapping suggest that ITGB1 may be a direct target of miR-183. The negative correlation between miR-183 and ITGB1 expression in prostate cancer cohorts supports their interaction in the clinical set. Overall, cell adhesion was uncovered as a major pathway controlled by miR-183 in prostate cancer, and ITGB1 was identified as a relevant mediator of this effect.
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Niu, Yaqian, Fang Liu, Xiuyue Wang, Yuling Chang, Yanmei Song, Huiyuan Chu, Shisan Bao, and Che Chen. "miR-183-5p Promotes HCC Migration/Invasion via Increasing Aerobic Glycolysis." OncoTargets and Therapy Volume 14 (June 2021): 3649–58. http://dx.doi.org/10.2147/ott.s304117.
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Rong, Hui, Hanwei Jiao, Yongchang Hao, Feng Pang, Guohua Li, Dongmei Peng, Yaying Li, et al. "CD14 gene silencing alters the microRNA expression profile of RAW264.7 cells stimulated by Brucella melitensis infection." Innate Immunity 23, no. 5 (April 26, 2017): 424–31. http://dx.doi.org/10.1177/1753425917707025.
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Innate recognition of Brucella spp. is a key step in the activation of inflammation. CD14 binds PAMPs and is involved in LPS-induced pro-inflammatory cytokine release. Previously we showed that knock down of CD14 in RAW264.7 macrophages disrupted Brucella–host interactions. However, its effect on the macrophage microRNA (miRNA) expression profile, especially after stimulation by Brucella infection, is still unclear. To identify miRNAs involved in the macrophage response to Brucella infection, we performed miRNA expression profiling of CD14 knock-down RAW264.7 (224.3) macrophages infected with Brucella melitensis, and demonstrated, for the first time, that CD14 knock down significantly up-regulated the expression of mmu-miR-199a-3p and mmu-miR-183-5p in these conditions. These miRNAs have a well-characterized association with the target genes involved in immune response, inflammatory response, innate immune response, apoptosis processes, anti-apoptosis, cytokine production and cytokine-mediated signaling pathways. Among the 104 inflammation-related candidate target genes of mmu-miR-199a-3p and mmu-miR-183-5p in the 224.3+ B. melitensis group cells, the expression of the Cbl-b, a potential target of mmu-miR-199a-3p, was confirmed to be down-regulated using qRT-PCR and Western blot analysis. Our findings suggest that CD14 functions in the Brucella–host interaction may be through altered miRNA expression, and regulation of Cbl-b proteins.
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Sedgeman, Leslie R., Carine Beysen, Ryan M. Allen, Marisol A. Ramirez Solano, Scott M. Turner, and Kasey C. Vickers. "Intestinal bile acid sequestration improves glucose control by stimulating hepatic miR-182-5p in type 2 diabetes." American Journal of Physiology-Gastrointestinal and Liver Physiology 315, no. 5 (November 1, 2018): G810—G823. http://dx.doi.org/10.1152/ajpgi.00238.2018.
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Colesevelam is a bile acid sequestrant approved to treat both hyperlipidemia and type 2 diabetes, but the mechanism for its glucose-lowering effects is not fully understood. The aim of this study was to investigate the role of hepatic microRNAs (miRNAs) as regulators of metabolic disease and to investigate the link between the cholesterol and glucose-lowering effects of colesevelam. To quantify the impact of colesevelam treatment in rodent models of diabetes, metabolic studies were performed in Zucker diabetic fatty (ZDF) rats and db/db mice. Colesevelam treatments significantly decreased plasma glucose levels and increased glycolysis in the absence of changes to insulin levels in ZDF rats and db/db mice. High-throughput sequencing and real-time PCR were used to quantify hepatic miRNA and mRNA changes, and the cholesterol-sensitive miR-96/182/183 cluster was found to be significantly increased in livers from ZDF rats treated with colesevelam compared with vehicle controls. Inhibition of miR-182 in vivo attenuated colesevelam-mediated improvements to glycemic control in db/db mice. Hepatic expression of mediator complex subunit 1 (MED1), a nuclear receptor coactivator, was significantly decreased with colesevelam treatments in db/db mice, and MED1 was experimentally validated to be a direct target of miR-96/182/183 in humans and mice. In summary, these results support that colesevelam likely improves glycemic control through hepatic miR-182–5p, a mechanism that directly links cholesterol and glucose metabolism. NEW & NOTEWORTHY Colesevelam lowers systemic glucose levels in Zucker diabetic fatty rats and db/db mice and increases hepatic levels of the sterol response element binding protein 2-responsive microRNA cluster miR-96/182/183. Inhibition of miR-182 in vivo reverses the glucose-lowering effects of colesevelam in db/db mice. Mediator complex subunit 1 (MED1) is a novel, direct target of the miR-96/182/183 cluster in mice and humans.
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Zhang, Tianxiang, Wei Li, Meng Gu, Ziyu Wang, Shijie Zhou, Xuefeng Hao, Weiying Li, and Shaofa Xu. "Clinical Significance of miR-183-3p and miR-182-5p in NSCLC and Their Correlation." Cancer Management and Research Volume 13 (April 2021): 3539–50. http://dx.doi.org/10.2147/cmar.s305179.
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Zhang, Aisen, Cheng Wang, Hui Lu, Xi Chen, Yi Ba, Chunni Zhang, and Chen-Yu Zhang. "Altered Serum MicroRNA Profile May Serve as an Auxiliary Tool for Discriminating Aggressive Thyroid Carcinoma from Nonaggressive Thyroid Cancer and Benign Thyroid Nodules." Disease Markers 2019 (September 16, 2019): 1–11. http://dx.doi.org/10.1155/2019/3717683.
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Thyroid cancers are the most common malignancy of the endocrine system; however, there is no reliable blood biomarkers for thyroid cancer diagnosis and even for aggressive and nonaggressive thyroid cancers as well as benign nodule discrimination. The present study is aimed at evaluating whether circulating microRNA (miRNA) can differentiate aggressive and nonaggressive thyroid cancer from benign thyroid nodules. In this study, we performed a multiphase, case-control study to screen serum miRNA expression profile in 100 patients with papillary thyroid cancer (PTC), 15 patients with aggressive medullary thyroid carcinoma (MTC), 91 patients with benign nodules, and 89 healthy controls using TaqMan low-density array followed by extensive reverse transcription quantitative real-time PCR validation. The results showed that the serum levels of miR-222-3p, miR-17-5p, and miR-451a were markedly increased, while miR-146a-5p, miR-132-3p, and miR-183-3p were significantly decreased in the PTC and benign nodule groups compared with the control group. There was no difference in the miRNA expression profile between the PTC group and the benign nodule group. Nevertheless, the serum levels of miR-222-3p and miR-17-5p were significantly increased in the MTC group than the benign nodule and control group. Moreover, receiver operating characteristic curve analyses demonstrated that the 2 miRNAs and their panel can accurately discriminate MTC from the benign nodule group and healthy controls. These findings indicated that the altered circulating miRNAs may discriminate PTC and benign thyroid nodules from controls, and serum miR-222-3p and miR-17-5p have the potential to serve as auxiliary tools for diagnosing more aggressive thyroid carcinomas, such as MTC.
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Han, Hui, Shenkang Zhou, Gengzhen Chen, Yandi Lu, and Hui Lin. "ABAT targeted by miR-183-5p regulates cell functions in liver cancer." International Journal of Biochemistry & Cell Biology 141 (December 2021): 106116. http://dx.doi.org/10.1016/j.biocel.2021.106116.
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Bueno Marinas, Maria, Rudy Celeghin, Marco Cason, Riccardo Bariani, Anna Chiara Frigo, Joanna Jager, Petros Syrris, et al. "A microRNA Expression Profile as Non-Invasive Biomarker in a Large Arrhythmogenic Cardiomyopathy Cohort." International Journal of Molecular Sciences 21, no. 4 (February 24, 2020): 1536. http://dx.doi.org/10.3390/ijms21041536.
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Arrhythmogenic Cardiomyopathy (AC) is a clinically and genetically heterogeneous myocardial disease. Half of AC patients harbour private desmosomal gene variants. Although microRNAs (miRNAs) have emerged as key regulator molecules in cardiovascular diseases and their involvement, correlated to phenotypic variability or to non-invasive biomarkers, has been advanced also in AC, no data are available in larger disease cohorts. Here, we propose the largest AC cohort unbiased by technical and biological factors. MiRNA profiling on nine right ventricular tissue, nine blood samples of AC patients, and four controls highlighted 10 differentially expressed miRNAs in common. Six of these were validated in a 90-AC patient cohort independent from genetic status: miR-122-5p, miR-133a-3p, miR-133b, miR-142-3p, miR-182-5p, and miR-183-5p. This six-miRNA set showed high discriminatory diagnostic power in AC patients when compared to controls (AUC-0.995), non-affected family members of AC probands carrying a desmosomal pathogenic variant (AUC-0.825), and other cardiomyopathy groups (Hypertrophic Cardiomyopathy: AUC-0.804, Dilated Cardiomyopathy: AUC-0.917, Brugada Syndrome: AUC-0.981, myocarditis: AUC-0.978). AC-related signalling pathways were targeted by this set of miRNAs. A unique set of six-miRNAs was found both in heart-tissue and blood samples of AC probands, supporting its involvement in disease pathogenesis and its possible role as a non-invasive AC diagnostic biomarker.
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Meerson, Ari, Azwar Najjar, Elias Saad, Wisam Sbeit, Masad Barhoum, and Nimer Assy. "Sex Differences in Plasma MicroRNA Biomarkers of Early and Complicated Diabetes Mellitus in Israeli Arab and Jewish Patients." Non-Coding RNA 5, no. 2 (April 5, 2019): 32. http://dx.doi.org/10.3390/ncrna5020032.
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MicroRNAs play functional roles in the etiology of type 2 diabetes mellitus (T2DM) and complications, and extracellular microRNAs have attracted interest as potential biomarkers of these conditions. We aimed to identify a set of plasma microRNAs, which could serve as biomarkers of T2DM and complications in a mixed Israeli Arab/Jewish patient sample. Subjects included 30 healthy volunteers, 29 early-stage T2DM patients, and 29 late-stage T2DM patients with renal and/or vascular complications. RNA was isolated from plasma, and the levels of 12 candidate microRNAs were measured by quantitative reverse transcription and polymerase chain reaction (qRT-PCR). MicroRNA levels were compared between the groups and correlated to clinical measurements, followed by stepwise regression analysis and discriminant analysis. Plasma miR-486-3p and miR-423 were respectively up- and down-regulated in T2DM patients compared to healthy controls. MiR-28-3p and miR-423 were up-regulated in patients with complicated T2DM compared to early T2DM, while miR-486-3p was down-regulated. Combined, four microRNAs (miR-146a-5p, miR-16-2-3p, miR-126-5p, and miR-30d) could distinguish early from complicated T2DM with 77% accuracy and 79% sensitivity. In male patients only, the same microRNAs, with the addition of miR-423, could distinguish early from complicated T2DM with 83.3% accuracy. Furthermore, plasma microRNA levels showed significant correlations with clinical measurements, and these differed between men and women. Additionally, miR-183-5p levels differed significantly between the ethnic groups. Our study identified a panel of specific plasma microRNAs which can serve as biomarkers of T2DM and its complications and emphasizes the importance of sex differences in their clinical application.
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Tiwari, Anshul, Brian D. Hobbs, Jiang Li, Alvin T. Kho, Samir Amr, Juan C. Celedón, Scott T. Weiss, Craig P. Hersh, Kelan G. Tantisira, and Michael J. McGeachie. "Blood miRNAs Are Linked to Frequent Asthma Exacerbations in Childhood Asthma and Adult COPD." Non-Coding RNA 8, no. 2 (April 3, 2022): 27. http://dx.doi.org/10.3390/ncrna8020027.
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MicroRNAs have been independently associated with asthma and COPD; however, it is unclear if microRNA associations will overlap when evaluating retrospective acute exacerbations. Objective: We hypothesized that peripheral blood microRNAs would be associated with retrospective acute asthma exacerbations in a pediatric asthma cohort and that such associations may also be relevant to acute COPD exacerbations. Methods: We conducted small-RNA sequencing on 374 whole-blood samples from children with asthma ages 6–14 years who participated in the Genetics of Asthma in Costa Rica Study (GACRS) and 450 current and former adult smokers with and without COPD who participated in the COPDGene study. Measurements and Main Results: After QC, we had 351 samples and 649 microRNAs for Differential Expression (DE) analysis between the frequent (n = 183) and no or infrequent exacerbation (n = 168) groups in GACRS. Fifteen upregulated miRs had odds ratios (OR) between 1.22 and 1.59 for a doubling of miR counts, while five downregulated miRs had ORs between 0.57 and 0.8. These were assessed for generalization in COPDGene, where three of the upregulated miRs (miR-532-3p, miR-296-5p, and miR-766-3p) and two of the downregulated miRs (miR-7-5p and miR-451b) replicated. Pathway enrichment analysis showed MAPK and PI3K-Akt signaling pathways were strongly enriched for target genes of DE miRNAs and miRNAs generalizing to COPD exacerbations, as well as infection response pathways to various pathogens. Conclusion: miRs (451b; 7-5p; 532-3p; 296-5p and 766-3p) associated with both childhood asthma and adult COPD exacerbations may play a vital role in airflow obstruction and exacerbations and point to shared genomic regulatory machinery underlying exacerbations in both diseases.
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Yang, Qi, Bo Wei, Chuangang Peng, Le Wang, and Chang Li. "Identification of serum exosomal miR-98–5p, miR-183–5p, miR-323–3p and miR-19b-3p as potential biomarkers for glioblastoma patients and investigation of their mechanisms." Current Research in Translational Medicine 70, no. 1 (January 2022): 103315. http://dx.doi.org/10.1016/j.retram.2021.103315.
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Sun, Guangli, Gang Su, Fang Liu, and Wenjie Han. "NRAS Contributes to Retinoblastoma Progression Through SNHG16/miR-183-5p/NRAS Regulatory Network." OncoTargets and Therapy Volume 12 (December 2019): 10703–15. http://dx.doi.org/10.2147/ott.s232470.
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Guo, Ruowen, and Yide Qin. "LEMD1-AS1 Suppresses Ovarian Cancer Progression Through Regulating miR-183-5p/TP53 Axis." OncoTargets and Therapy Volume 13 (July 2020): 7387–98. http://dx.doi.org/10.2147/ott.s250850.
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Shang, Anquan, Xuan Wang, Chenzheng Gu, Wenfang Liu, Junjun Sun, Bingjie Zeng, Chen Chen, et al. "Exosomal miR-183-5p promotes angiogenesis in colorectal cancer by regulation of FOXO1." Aging 12, no. 9 (May 3, 2020): 8352–71. http://dx.doi.org/10.18632/aging.103145.
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Xu, Yuting, Chen Qiao, Siying He, Chen Lu, Shiqi Dong, Xiying Wu, Ming Yan, and Fang Zheng. "Identification of Functional Genes in Pterygium Based on Bioinformatics Analysis." BioMed Research International 2020 (November 20, 2020): 1–11. http://dx.doi.org/10.1155/2020/2383516.
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Purpose. The competing endogenous RNA (ceRNA) network regulatory has been investigated in the occurrence and development of many diseases. This research aimed at identifying the key RNAs of ceRNA network in pterygium and exploring the underlying molecular mechanism. Methods. Differentially expressed long noncoding RNAs (lncRNAs), microRNAs (miRNAs), and mRNAs were obtained from the Gene Expression Omnibus (GEO) database and analyzed with the R programming language. LncRNA and miRNA expressions were extracted and pooled by the GEO database and compared with those in published literature. The lncRNA-miRNA-mRNA network was constructed of selected lncRNAs, miRNAs, and mRNAs. Metascape was used to perform Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses on mRNAs of the ceRNA network and to perform Protein-Protein Interaction (PPI) Network analysis on the String website to find candidate hub genes. The Comparative Toxicogenomic Database (CTD) was used to find hub genes closely related to pterygium. The differential expressions of hub genes were verified using the reverse transcription-real-time fluorescent quantitative PCR (RT-qPCR). Result. There were 8 lncRNAs, 12 miRNAs, and 94 mRNAs filtered to construct the primary ceRNA network. A key lncRNA LIN00472 ranking the top 1 node degree was selected to reconstruct the LIN00472 network. The GO and KEGG pathway enrichment showed the mRNAs in ceRNA networks mainly involved in homophilic cell adhesion via plasma membrane adhesion molecules, developmental growth, regulation of neuron projection development, cell maturation, synapse assembly, central nervous system neuron differentiation, and PID FOXM1 PATHWAY. According to the Protein-Protein Interaction Network (PPI) analysis on mRNAs in LINC00472 network, 10 candidate hub genes were identified according to node degree ranking. Using the CTD database, we identified 8 hub genes closely related to pterygium; RT-qPCR verified 6 of them were highly expressed in pterygium. Conclusion. Our research found LINC00472 might regulate 8 hub miRNAs (miR-29b-3p, miR-183-5p, miR-138-5p, miR-211-5p, miR-221-3p, miR-218-5p, miR-642a-5p, miR-5000-3p) and 6 hub genes (CDH2, MYC, CCNB1, RELN, ERBB4, RB1) in the ceRNA network through mainly PID FOXM1 PATHWAY and play an important role in the development of pterygium.
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Zhang, Jin, Renqing Nie, Mengxi Liu, and Xiaoyi Zhang. "A Novel Strategy for Identifying NSCLC MicroRNA Biomarkers and Their Mechanism Analysis Based on a Brand-New CeRNA-Hub-FFL Network." International Journal of Molecular Sciences 23, no. 19 (September 25, 2022): 11303. http://dx.doi.org/10.3390/ijms231911303.
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Finding reliable miRNA markers and revealing their potential mechanisms will play an important role in the diagnosis and treatment of NSCLC. Most existing computational methods for identifying miRNA biomarkers only consider the expression variation of miRNAs or rely heavily on training sets. These deficiencies lead to high false-positive rates. The independent regulatory model is an important complement to traditional models of co-regulation and is more impervious to the dataset. In addition, previous studies of miRNA mechanisms in the development of non-small cell lung cancer (NSCLC) have mostly focused on the post-transcriptional level and did not distinguish between NSCLC subtypes. For the above problems, we improved mainly in two areas: miRNA identification based on both the NOG network and biological functions of miRNA target genes; and the construction of a 4-node directed competitive regulatory network to illustrate the mechanisms. NSCLC was classified as lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) in this work. One miRNA biomarker of LUAD (miR-708-5p) and four of LUSC (miR-183-5p, miR-140-5p, miR-766-5p, and miR-766-3p) were obtained. They were validated using literature and external datasets. The ceRNA-hub-FFL involving transcription factors (TFs), microRNAs (miRNAs), mRNAs, and long non-coding RNAs (lncRNAs) was constructed. There were multiple interactions among these components within the net at the transcriptional, post-transcriptional, and protein levels. New regulations were revealed by the network. Meanwhile, the network revealed the reasons for the previous conflicting conclusions on the roles of CD44, ACTB, and ITGB1 in NSCLC, and demonstrated the necessity of typing studies on NSCLC. The novel miRNA markers screening method and the 4-node directed competitive ceRNA-hub-FFL network constructed in this work can provide new ideas for screening tumor markers and understanding tumor development mechanisms in depth.
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Pirola, Carlos J., and Silvia Sookoian. "MicroRNAs as messengers of liver diseases: has the message finally been decrypted?" Clinical Science 136, no. 5 (March 2022): 323–28. http://dx.doi.org/10.1042/cs20211177.
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Abstract MicroRNAs (miRNAs), which are regarded as crucial regulators of gene expression and diverse aspects of cell biology, can be present in various body fluids as highly stable molecules. It is also known that miRNAs exert tissue-specific regulation of gene transcription. Large amount of clinical and experimental evidence provided the rationale for raising the intriguing question of whether miRNAs can mediate cell–cell communication. For those reasons, miRNAs have been considered as the ‘Holy Grail’ of biomarkers allowing non-invasive diagnostic screening and early detection of a variety of diseases, including solid and non-solid cancers. In a study published in Clin. Sci. (Lond.) (2011) 120(5):183–193 (https://doi.org/10.1042/CS20100297), Gui et al. investigated the hypothesis that circulating miRNAs could be used to identify patients with liver pathologies. Specifically, the authors profiled circulating miRNAs in patients with hepatocellular carcinoma (HCC), liver cirrhosis (LC), and healthy controls and found that serum miR-885-5p levels were significantly higher in samples of patients with HCC (6.5-fold increase) and LC (8.8-fold increase). In this commentary, we highlight biological aspects associated with mir-122-the ‘liver-specific’ miRNA, which has been associated with a diverse range of liver pathologies. In addition, we discuss the relevance of mir-885-5p as potential biomarker for detecting human cancers. Finally, we provide some clues about how presumably unrelated miRNAs such as miR-122 and miR-885-5p may act in similar biological processes (BPs), making the miRNA regulatory networks more complex than anticipated.
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Li, Jia, Zhi-Qiang Hu, Song-Yang Yu, Li Mao, Zheng-Jun Zhou, Peng-Cheng Wang, Yu Gong, et al. "CircRPN2 Inhibits Aerobic Glycolysis and Metastasis in Hepatocellular Carcinoma." Cancer Research 82, no. 6 (March 15, 2022): 1055–69. http://dx.doi.org/10.1158/0008-5472.can-21-1259.
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Abstract Although circular RNAs (circRNA) are known to modulate tumor initiation and progression, their role in hepatocellular carcinoma (HCC) metastasis remains poorly understood. Here, three metastasis-associated circRNAs identified in a previous circRNA-sequencing study were screened and validated in two HCC cohorts. CircRPN2 was downregulated in highly metastatic HCC cell lines and HCC tissues with metastasis. Patients with HCC with lower circRPN2 levels displayed shorter overall survival and higher rates of cumulative recurrence. Mechanistic studies in vitro and in vivo revealed that circRPN2 binds to enolase 1 (ENO1) and accelerates its degradation to promote glycolytic reprogramming through the AKT/mTOR pathway, thereby inhibiting HCC metastasis. CircRPN2 also acted as a competing endogenous RNA for miR-183–5p, which increases forkhead box protein O1 (FOXO1) expression to suppress glucose metabolism and tumor progression. In clinical samples, circRPN2 expression negatively correlated with ENO1 and positively correlated with FOXO1, and expression of circRPN2, either alone or in combination with ENO1 and FOXO1, was a novel indicator of HCC prognosis. These data support a model wherein circRPN2 inhibits HCC aerobic glycolysis and metastasis via acceleration of ENO1 degradation and regulation of the miR-183–5p/FOXO1 axis, suggesting that circRPN2 represents a possible therapeutic target in HCC. Significance: The circRNA circRPN2 is a potential prognostic biomarker and therapeutic target in hepatocellular carcinoma that suppresses aerobic glycolysis and metastasis.
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Eminaga, Okyaz, Jochen Fries, Fabian Woetzel, Susanne Neiss, Ute Warnecke-Eberz, Michaela Heitmann, and Axel Heidenreich. "The expression profiles of miRNAs in the progression of prostate cancer from high-grade prostatic intraepithelial neoplasia to metastatic diseases." Journal of Clinical Oncology 34, no. 2_suppl (January 10, 2016): 221. http://dx.doi.org/10.1200/jco.2016.34.2_suppl.221.
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221 Background: The epigenetic regulation by miRNA plays an important role in tumor progression of prostate cancer (PCa). Methods: The expression data of 1054 miRNAs from TCGA were applied to identify relevant miRNAs associated with tumor progression (i.e. miR-210, miR-375, miR-378, miR-345, miR-143 miR-183 and miR-98). miRNA were isolated by miRNeasy FFPE kit (Qiagen, Hilden, Germany) from paraffin-embedded tissues of prostate specimens with PCa, HGPIN and normal tissues. Early-stage PCa was defined as PCa with pT2 tumor stage, Gleason score < = 7a (3+4) and PSA level < 10 ng/ml. PCa with pT3/4 or Gleason > 7a was defined as advanced PCa. PCa with pN1 were considered as metastatic diseases. Additionally, 3 cases with castration-resistant prostate cancer (CRPC) were considered. Quantitative miRNA expression data were acquired and analyzed using a real-time TaqMan-based PCR. ANOVA analyses were performed to evaluate the expression of miRNAs between HGPIN, Normal and PCa tissues. The small nuclear U6 RNA was used as an endogenous control Results: ANOVA analysis revealed a significant variation in expression of all miRNAs among groups. The expression level of miR-183 and miR-375 increased with the tumor progression. miR-143, miR-375-3p were inversely correlated with the tumor progression. miR-210 and miR-183 were significantly overexpressed in metastatic diseases compared to non-metastatic diseases (FDR < 0.01), whereas the expression level of miR-378-3p was lower in metastatic diseases than in organ-confined PCa. The expression of miR-98 was lower in PCa compared to normal tissues. In silico analysis, the down-regulation of miR-98 and miR-345-5p seems to activate the HIF-1 signaling pathway initiating the up-regulation of miR-210 that interact with genes related to cell cycle, RNA transcription, homologous recombination and non-homologous end-joining. Conclusions: Our data reveal epigenetic regulations of miRNA, which are associated with transition from normal tissues to HGIPN, from HGPIN to early-stage PCa, and early-stage PCa to advanced PCa. Advanced PCa represents the first stage of metastatic diseases.
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Jin, Lin, Yue Luo, Ying-Chun Zhao, and Hai Tao. "MiR-183-5p Promotes Tumor Progression of Osteosarcoma and Predicts Poor Prognosis in Patients." Cancer Management and Research Volume 13 (January 2021): 805–14. http://dx.doi.org/10.2147/cmar.s285909.
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Zhou, Shaolan, Jing Zhang, Pengfei Luan, Zhanbing Ma, Jie Dang, Hong Zhu, Qian Ma, Yanfeng Wang, and Zhenghao Huo. "Corrigendum to “miR-183-5p Is a Potential Molecular Marker of Systemic Lupus Erythematosus”." Journal of Immunology Research 2021 (September 4, 2021): 1–2. http://dx.doi.org/10.1155/2021/9818203.
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Zheng, Zhuojun, Xiao Zheng, Yuandong Zhu, Xiaoyan Gu, Weiying Gu, Xiaobao Xie, Wenwei Hu, and Jingting Jiang. "miR-183-5p Inhibits Occurrence and Progression of Acute Myeloid Leukemia via Targeting Erbin." Molecular Therapy 27, no. 3 (March 2019): 542–58. http://dx.doi.org/10.1016/j.ymthe.2019.01.016.
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Meng, Fanlu, and Linlin Zhang. "miR-183-5p functions as a tumor suppressor in lung cancer through PIK3CA inhibition." Experimental Cell Research 374, no. 2 (January 2019): 315–22. http://dx.doi.org/10.1016/j.yexcr.2018.12.003.
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