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Journal articles on the topic 'MiR-544a'

Author: Grafiati

Published: 14 March 2023

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1

Yang, Lei, Dawei Ge, Xi Chen, Chunzhi Jiang, and Shengnai Zheng. "miRNA-544a Regulates the Inflammation of Spinal Cord Injury by Inhibiting the Expression of NEUROD4." Cellular Physiology and Biochemistry 51, no. 4 (2018): 1921–31. http://dx.doi.org/10.1159/000495717.

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Background/Aims: To explore the potential role of miR-544a in spinal cord injury and the possible mechanism involved. Methods: We established a mouse model with spinal cord injury to examine the changes in grip force recovery of the forelimb or the posterior limb of the mouse. Microarray was performed to achieve differentiated miRNAs in the mice. The expressions of miR-544a, MCP-1, IL36B and IL17B after spinal cord injury were detected by qRT-PCR. Subsequently, miR-544a was overexpressed to observe changes in inflammation and grip strength after spinal cord injury. Target gene of miR-544a was then predicted using bioinformatics technology. Finally, dual luciferase reporter gene assay was used to verify the binding of miR-544a to its target gene. Results: Using mice models with spinal cord injury, we found that the strength of their four limbs began to recover 7 days after injury. The results of microarray and qRT-PCR confirmed that mir-544a level in mice with spinal cord injury decreased with increase of injury time, while the levels of inflammatory genes MCP-1 (monocyte chemoattractant protein-1), IL1 (interleukin-1) and TNF-α (tumor necrosis factor alpha) IL36B (interleukin-36 beta) and IL17B (interleukin-17 beta) were significantly increased. However, overexpression of miR-544a in the mice significantly reduced the level of inflammation and restored their grip strength in their four limbs. Finally, we found that miR-544a can bind to the NEUROD4 (Neurogenic differentiation 4) 3’UTR (Untranslated Region) region through bioinformatics website prediction, which was further confirmed by dual luciferase reporter assay. NEUROD4 level was significantly reduced following the overexpression of miR-544a. Conclusion: The expression of miR-544a was significantly decreased after spinal cord injury. High expression of miR-544a could alleviate the inflammation caused by spinal cord injury and promote the recovery of spinal cord via the inhibition of NEUROD4.

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2

Alsaadoni, Hani, Burcu Çaykara, Sadrettin Pençe, Halime Hanım Pençe, and Süleyman Bademler. "The expression levels of miR-655-3p, miR127-5p, miR-369-3p, miR-544a in gastric cancer." Turkish Journal of Biochemistry 44, no. 4 (August 23, 2019): 487–91. http://dx.doi.org/10.1515/tjb-2019-0057.

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Abstract Background Gastric cancer, one of the most common cancers in the world, is a multifactorial disease in which environmental and genetic factors play a role. In our study, we aimed to determine the expression levels of four miRNAs (miR127-5p, miR-544a, miR-369-3p and miR-655-3p) on chromosome 14q32 in gastric cancer. Materials and methods Total RNA was isolated from blood samples taken from 66 gastric cancer and 66 healthy individuals. The gene expression levels determined by cDNA and quantitative real-time polymerase chain reaction were analyzed according to the 2−∆∆Ct method. SPSS 22 were used for statistical analysis and p < 0.05 was considered as statistically significant. Results and discussion miR-655-3p (fold change: 100, p = 0.026), miR-127-5p (fold change: 48, p < 0.001) and miR-369-3p (fold change: 1.6, p > 0.05) was less expressed in the gastric cancer group than control group. miR-544a was found 15.5-fold more expressed in the patient group than control group (fold change: 15.47, p < 0.001). Conclusion miR127-5p, miR-544a, and miR-655-3p may be evaluated as biomarkers in gastric cancer.

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3

Pan, Lingxiao, and Kaifeng Gan. "MiR-544a Regulates Synovial Cell Proliferation, Invasion, Migration and Apoptosis by Targeting E2F2." Journal of Biomaterials and Tissue Engineering 9, no. 8 (August 1, 2019): 1065–72. http://dx.doi.org/10.1166/jbt.2019.2108.

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In the present study, we aimed to explore the role of MiR-544a in inhibiting the proliferation and promoting apoptosis of rheumatoid arthritis synovial cells. Detected the expression of MiR-544 and E2F2 in Normal Fibroblast-like synoviocytes (NFLs) and Rheumatoid arthritis Fibroblast-like synoviocytes (RA-FLSs) by RT-qPCR and western blot. The target genes of MiR-544a were predicted by miRDB and were verified with the luciferase reporter system and western blot. The E2F2 overexpression plasmid was constructed and transfected into RAFLS. Cell apoptosis were detected by CCK-8. Wound healing and transwell assay were employed to detect cell invasion ability. The expression of E2F2, MMP2 and MMP9 were measured by Western blot. Further, the level of apoptosis and live cells were detected by flow cytometry DAPI staining, respectively. The expression of cell proliferation, apoptosis and migration-related proteins were detected by Western blot. The expression of miR-544 in RA-FLSs is significantly lower than that in NFLs and E2F2 is increased in RA-FLSs. E2F2 is one of the target genes of miR-544a by miRDB detection and luciferase activity assay. Overexpression of miR-544 inhibits cell proliferation, invasion, migration and apoptosis by targeting E2F2 in RA-FLSs. MiR-544a regulates synovial cell proliferation, invasion, migration and apoptosis by targeting E2F2, which is expected to be an attractive target for the development of new drugs for the treatment of rheumatoid arthritis.

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4

Potenza, Nicoletta, Filomena Castiello, Marta Panella, Giovanni Colonna, Gennaro Ciliberto, Aniello Russo, and Susan Costantini. "Human MiR-544a Modulates SELK Expression in Hepatocarcinoma Cell Lines." PLOS ONE 11, no. 6 (June 8, 2016): e0156908. http://dx.doi.org/10.1371/journal.pone.0156908.

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5

Stella di Stadio, Chiara, Raffaella Faraonio, Antonella Federico, Filomena Altieri, Emilia Rippa, and Paolo Arcari. "GKN1 expression in gastric cancer cells is negatively regulated by miR-544a." Biochimie 167 (December 2019): 42–48. http://dx.doi.org/10.1016/j.biochi.2019.09.005.

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6

Lu, Pengwei, Yuanting Gu, Lin Li, Fang Wang, and Xinguang Qiu. "miR-544a Promotes Breast Cancer Cell Migration and Invasion Reducing Cadherin 1 Expression." Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 23, no. 4 (March 25, 2016): 165–70. http://dx.doi.org/10.3727/096504016x14519157902726.

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7

Azari, Hanieh, Elham Karimi, Mohammad Shekari, Ahmad Tahmasebi, Amin Reza Nikpoor, Ahmad Agha Negahi, Nima Sanadgol, and Pegah Mousavi. "Construction of a lncRNA–miRNA–mRNA network to determine the key regulators of the Th1/Th2 imbalance in multiple sclerosis." Epigenomics 13, no. 22 (November 2021): 1797–815. http://dx.doi.org/10.2217/epi-2021-0296.

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Aim: The exact epigenetic mechanisms that determine the balance of T helper (Th)1 and Th2 cells and autoimmune responses in multiple sclerosis (MS) remain unclear. We aim to clarify these. Methods: A combination of bioinformatics analysis and molecular evaluations was utilized to identify master hub genes. Results: A competitive endogenous RNA network containing six long noncoding RNAs (lncRNAs), 21 miRNAs and 86 mRNAs was provided through enrichment analysis and a protein–protein interaction network. NEAT1 and MALAT1 were found as differentially expressed lncRNAs using Gene Expression Omnibus (GSE21942). Quantitative real-time PCR results demonstrate dysregulation in the RUNX3 (a regulator of Th1/Th2 balance), GATA3 and TBX21, as well as miR-544a and miR-210-3p (which directly target RUNX3). ELISA also confirmed an imbalance in IFN-γ (Th1)/IL-4 (Th2) in MS patients. Conclusion: Our findings introduce novel biomarkers leading to Th1/Th2 imbalance in MS.

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8

De Palma, A., C. Heluany, A. Fioravanti, I. Clark, and G. Nalesso. "MIR-544A: A NEW MODULATOR OF THE WNT/β-CATENIN PATHWAY IN ARTICULAR CHONDROCYTES." Osteoarthritis and Cartilage 30 (April 2022): S169. http://dx.doi.org/10.1016/j.joca.2022.02.220.

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9

Liu, Xiaochun, Jing Ma, Feng Xu, and Li Li. "TINCR suppresses proliferation and invasion through regulating miR-544a/FBXW7 axis in lung cancer." Biomedicine & Pharmacotherapy 99 (March 2018): 9–17. http://dx.doi.org/10.1016/j.biopha.2018.01.049.

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10

He, Qianru, Lini Zhao, Yunhui Liu, Xiaobai Liu, Jian Zheng, Hai Yu, Heng Cai, et al. "circ-SHKBP1 Regulates the Angiogenesis of U87 Glioma-Exposed Endothelial Cells through miR-544a/FOXP1 and miR-379/FOXP2 Pathways." Molecular Therapy - Nucleic Acids 10 (March 2018): 331–48. http://dx.doi.org/10.1016/j.omtn.2017.12.014.

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11

MO, XIAO-MEI, HUA-HUI LI, MING LIU, and YAN-TUAN LI. "Downregulation of GSK3β by miR-544a to maintain self-renewal ability of lung caner stem cells." Oncology Letters 8, no. 4 (July 28, 2014): 1731–34. http://dx.doi.org/10.3892/ol.2014.2387.

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12

Wang, Ansheng, Chengling Zhao, Yuan Gao, Guixin Duan, Yuming Yang, Bo Fan, Xiaojing Wang, and Kangwu Wang. "LEF1-AS1 contributes to proliferation and invasion through regulating miR-544a/ FOXP1 axis in lung cancer." Investigational New Drugs 37, no. 6 (February 8, 2019): 1127–34. http://dx.doi.org/10.1007/s10637-018-00721-z.

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13

Zheng, Wei-Ping, Fan-Long Meng, and Lian-Yun Wang. "miR-544a Stimulates endometrial carcinoma growth via targeted inhibition of reversion-inducing cysteine-rich protein with Kazal motifs." Molecular and Cellular Probes 53 (October 2020): 101572. http://dx.doi.org/10.1016/j.mcp.2020.101572.

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14

Liu, Yong, Chuanping Yang, Chengsong Cao, Qing Li, Xin Jin, and Hanping Shi. "Hsa_circ_RNA_0011780 Represses the Proliferation and Metastasis of Non-Small Cell Lung Cancer by Decreasing FBXW7 via Targeting miR-544a." OncoTargets and Therapy Volume 13 (January 2020): 745–55. http://dx.doi.org/10.2147/ott.s236162.

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15

Marinović, Sonja, Anita Škrtić, Tina Catela Ivković, Mirko Poljak, and Sanja Kapitanović. "Regulation of KRAS protein expression by miR-544a and KRAS-LCS6 polymorphism in wild-type KRAS sporadic colon adenocarcinoma." Human Cell 34, no. 5 (July 7, 2021): 1455–65. http://dx.doi.org/10.1007/s13577-021-00576-2.

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16

Zhang, Lina, Changyong Zhou, Qiaoji Qin, Zhenfang Liu, and Peng Li. "LncRNA LEF1‐AS1 regulates the migration and proliferation of vascular smooth muscle cells by targeting miR‐544a/PTEN axis." Journal of Cellular Biochemistry 120, no. 9 (April 23, 2019): 14670–78. http://dx.doi.org/10.1002/jcb.28728.

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17

Liu, Yong, Chuanping Yang, Chengsong Cao, Qing Li, Xin Jin, and Hanping Shi. "Hsa_circ_RNA_0011780 Represses the Proliferation and Metastasis of Non-Small Cell Lung Cancer by Decreasing FBXW7 via Targeting miR-544a [Retraction]." OncoTargets and Therapy Volume 15 (November 2022): 1385–86. http://dx.doi.org/10.2147/ott.s397666.

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18

Ma, Xiaomin, Tao Ma, Long Chang, Xiaolei Chen, Gen Xia, Chen Li, and Huan Liu. "Correlation between miRNA-124, miRNA-544a, and TNF-α levels in acute spinal cord injury." Spinal Cord, March 16, 2022. http://dx.doi.org/10.1038/s41393-022-00763-4.

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Abstract Study design Retrospective. Objectives Acute spinal cord injury (ASCI) is caused by direct or indirect strikes from external forces on the spinal cord. Here, we investigated the correlation between the miR-124, miR-544a, and TNF-α levels in patients with ASCI, aiming to evaluate the potential usage of miR-124 and miR-544a in ASCI diagnosis. Setting University/hospital. Methods A total of 90 (58 male/32 female) ASIA patients and 15 (9 male/6 female) control patients (with acute limb trauma) were involved in the presented study. The ASIA patients were further subclustered based on the International Standards for the Neurological Classification of SCI (ISNCSCI) exam. 30 (18 male/12 female)cases were determined to have complete spinal cord injury (CSCI) and classified as ASIA grade A (Complete); 30 (20 male/10 female) cases were determined to have incomplete spinal cord injury (ISCI) and classified as ASIA grade B (sensory incomplete), C (motor incomplete), or D (motor incomplete); 30 (20 male/10 female) cases were determined to have normal neurological function (NNF) and classified as ASIA grade E (Normal). Plasma miR-124, miRNA-544a, and tumor necrosis factor-alpha (TNF-α) levels were measured from the blood samples collected 24 h, 48 h, and 72 h after trauma. Results The levels of miR-124 and miR-544a in the CSCI and ISCI groups were significantly higher than those of the NNF and the control group 24 h after injury (P < 0.05). The increased levels gradually declined from 24 h to 72 h after injury. The area under the receiver operating characteristic curve (ROC) of miR-124, miR-544a and TNF-α 24 h after trauma in patients with acute spinal cord injury were 0.948 [95% CI (0.890, 1.000)], 0.815 [95% CI (0.638, 0.994)] and 0.770 [95% CI (0.641, 0.879)], respectively. Conclusion The miRNA-124 and miRNA-544a levels increased significantly in ASCI patients compared with control patients 24 h after injury. These increased levels gradually reduced from 24 h to 72 h after injury. There is a strong positive correlation between miRNA-124, miRNA-544a, and acute spinal cord injury. Sponsorship The present study was supported by a University-level project of Ningxia Medical University (Project Number: XY2017147).

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19

Hater, Nina, Katharina M. Iwaniuk, Carina Leifeld, Pia Grüten, Constanze Wiek, Katharina Raba, Fan Zhang, et al. "Identification of new RAD51D-regulating microRNAs that also emerge as potent inhibitors of the Fanconi Anemia/homologous recombination pathways." Human Molecular Genetics, July 29, 2022. http://dx.doi.org/10.1093/hmg/ddac177.

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Abstract The Fanconi anemia (FA) and homologous recombination (HR) pathways, which partially overlap and include RAD51 and its paralogs, are key for the repair of different types of DNA damage, such as DNA interstrand crosslinks. Here, as a first step to broadly assess the impact of microRNA-mediated regulation, we examined microRNA expression profiles in five isogenic fibroblast cell pairs, either deficient in DNA repair due to germ-line mutations in FANCA, FANCB, FANCC, FANCI or BRIP1/FANCJ or proficient due to correction with retroviral vectors. In each pair, we observed lower abundance of specific microRNAs in the FA-deficient cells. From the list of microRNAs, we experimentally confirmed the effects of miR-141-3p and miR-369-3p targeting RAD51B and miR-15a-5p, miR-494-3p as well as miR-544a targeting RAD51D. However, by western blotting, only RAD51D protein was reduced by a mixture of its regulating microRNAs. Gene ontology analyses, and identification of additional FA/HR factors as targets of miR-15a-5p, miR-494-3p and miR-544a strongly suggested the widespread influence of these three microRNAs on HR. Interestingly, only miR-494-3p directly reduced RAD51 foci formation, while a mixture of miR-15a-5p, miR-494-3p and miR-544a strongly reduced HR activity in GFP repair assays. Summarized, by successfully employing this novel loss- and gain-of-function strategy, we have identified new microRNAs strongly inhibiting HR in mammalian cells. Understanding and modulating such miRNA regulation of DNA repair genes/pathways might help to overcome the reduced repair capacity of FA patients with bi-allelic hypomorphic mutations or help to engineer synthetic lethality strategies for patients with mutations in cancer-associated FA/HR genes.

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20

He, Wendan, Yanru Yang, Longgan Cai, Qiaoling Lei, Zhongdong Wang, and Xiaoxia Che. "MicroRNA expression profiles in peri-miniscrew implant crevicular fluid in orthodontics: a pilot study." BMC Oral Health 21, no. 1 (December 2021). http://dx.doi.org/10.1186/s12903-021-02009-w.

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Abstract Background This study systematically evaluated microRNA (miRNA) expression patterns in peri-miniscrew implant crevicular fluid (PMICF) in orthodontic patients. Methods Next-generation sequencing (NGS) was performed to obtain miRNA profiles in PMICF or gingival crevicular fluid (GCF) collected from 3 healthy volunteers (H), 3 peri-implantitis patients (PMSII) and 5 periodontitis patients (P). MiRNA expression patterns were compared between normal and orthodontic PMICF and GCF. Differentially expressed miRNAs were estimated by quantitative real-time PCR (qRT-PCR). Enrichment analyses of the gene targets controlled by these miRNAs were conducted by Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. Results Compared with healthy donors, in PMSII patients, a total of 206 upregulated miRNAs and 152 downregulated miRNAs were detected in PMICF, while periodontitis patients had 333 upregulated miRNAs and 318 downregulated miRNAs. MiR-544a, miR-1245b-3p, miR-1825, miR-4291, miR-3689e, and miR-4477a were chosen randomly for further examination. qRT-PCR examination confirmed that the expression levels of miR-1245b-3p and miR-4291 were higher in PMSII than in H samples and that the expression levels of miR-1825 were higher in PMSII than in P samples. However, contrary to the NGS results, qRT-PCR analysis showed decreased expression of miR544a in PMSII. MiR3689e and miR4477a expression did not differ significantly among all samples. According to GO and KEGG pathway analyses of miR-1825, miR-4291, and miR-1245b-3p high enrichment of target genes involved in the PI3K-AKT signalling pathway was observed. Conclusions The NGS analysis of normal and orthodontic PMICF/CGF showed different miRNA profiles, which may lay the foundation for future research on the molecular mechanism of PMSII. miR-4291, miR-1245b-3p and miR-1825 may be used as diagnostic markers and potential therapeutic targets for PMSII.

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21

Mo, Xiaomei, Fenghua Zhang, Hui Liang, Huahui Li, Haiping Xia, and Liu Ming. "miR-544a promotes the invasion of lung cancer cells by targeting cadherina 1 in vitro." OncoTargets and Therapy, June 2014, 895. http://dx.doi.org/10.2147/ott.s61695.

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