Relevant bibliographies by topics / MiR-198

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Academic literature on the topic 'MiR-198'

Author: Grafiati
Published: 6 September 2023

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Journal articles on the topic "MiR-198"

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Ray, Jessica, Christianne Hoey, Xiaoyong Huang, Paul Christopher Boutros, and Stanley K. Liu. "Microrna-198: A novel tumor suppressor in prostate cancer." Journal of Clinical Oncology 36, no. 6_suppl (February 20, 2018): 92. http://dx.doi.org/10.1200/jco.2018.36.6_suppl.92.

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92 Background: microRNAs (miRNAs) are small non-coding RNA molecules which act as repressors of gene function, and have been identified as playing substantial roles in cancer as both tumor suppressors and oncogenes. miR-198 has been reported to be down-regulated in several cancers, with low expression associated with worse overall survival. In addition, miR-198 has demonstrated tumor suppressor effects by altering several hallmarks of cancer. Despite compelling evidence in other cancers, miR-198's role in prostate cancer aggression has not yet been evaluated. Methods: Experiments were conducted by overexpressing miR-198 in three prostate cancer cell lines: DU145, LNCaP and 22RV1. To examine miR-198's effect on hallmarks of cancer in vitro, we used standard protocols to assay proliferation, colony formation, cell cycle profile, migration, and invasive potential. Gene array, qPCR, western blotting, and siRNA knockdown experiments were used to establish miR-198 downstream targets. Results: Overexpression of the candidate tumor suppressor miR-198 diminished proliferation in all prostate cancer cell lines and significantly impaired colony formation in soft agar. Subsequently, miR-198 expression was also demonstrated to reduce growth and tumor formation in vivo using LNCaP xenografts. Gene arrays and in silico target prediction identified several candidate targets, none of which have been previously linked to miR-198. MIB1, an E3 ubiquitin ligase, was the only target we have since identified to be reduced with miR-198 overexpression at both the RNA and protein levels. Knockdown of MIB1 recapitulated miR-198's effects on proliferation and colony formation, and further experiments are underway to demonstrate a direct binding relationship. An additional gene array with MIB1 siRNA will be performed to highlight pathways through which MIB1/miR-198 suppress tumorigenesis. Conclusions: Our evidence supports miR-198 as an important tumor suppressor in prostate cancer, with elevated expression impairing proliferation, colony formation, and in vivo tumor formation. This investigation into miR-198 highlights a potential role as a prostate cancer biomarker, or as a potential target of therapeutics to restore miRNA activity.
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Li, Siqi, Junmei Yang, Xiaoting Liu, Rui Guo, and Ruidong Zhang. "circITGA7 Functions as an Oncogene by Sponging miR-198 and Upregulating FGFR1 Expression in Thyroid Cancer." BioMed Research International 2020 (June 22, 2020): 1–8. http://dx.doi.org/10.1155/2020/8084028.

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Background. Emerging evidence has indicated that circular RNAs (circRNAs), recognized as functional noncoding transcripts in eukaryotic cells, may be involved in regulating many physiological or pathological processes. However, the regulation and function of circular RNA circITGA7 in thyroid cancer (TC) remains unknown. Methods. In this study, we found that circITGA7 is upregulated in TC cell lines. We then performed functional analyses in the cell lines to support clinical findings. Mechanistically, we demonstrated that circITGA7 can directly bind to miR-198 and reduce the inhibition effect of miR-198 on target FGFR1 expression. Results. We reported an upregulation of circITGA7 in patients with TC. Silencing of circITGA7 inhibits metastasis and proliferation of TC cell lines in vitro. In addition, in the TC cell lines, the knockdown of circITGA7 or overexpression of miR-198 significantly suppressed FGFR1 levels. Mechanistically, we found that circITGA7 acts as miR-198 competitive endogenous RNA (ceRNA) to regulate FGFR1 expression. Conclusions. In summary, circRNA circITGA7 may play a regulatory role in TC and may be a potential marker for TC diagnosis or progression.
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Sundaram, Gopinath M., Hisyam M. Ismail, Mohsin Bashir, Manish Muhuri, Candida Vaz, Srikanth Nama, Ghim Siong Ow, et al. "EGF hijacks miR-198/FSTL1 wound-healing switch and steers a two-pronged pathway toward metastasis." Journal of Experimental Medicine 214, no. 10 (August 21, 2017): 2889–900. http://dx.doi.org/10.1084/jem.20170354.

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Epithelial carcinomas are well known to activate a prolonged wound-healing program that promotes malignant transformation. Wound closure requires the activation of keratinocyte migration via a dual-state molecular switch. This switch involves production of either the anti-migratory microRNA miR-198 or the pro-migratory follistatin-like 1 (FSTL1) protein from a single transcript; miR-198 expression in healthy skin is down-regulated in favor of FSTL1 upon wounding, which enhances keratinocyte migration and promotes re-epithelialization. Here, we reveal a defective molecular switch in head and neck squamous cell carcinoma (HNSCC). This defect shuts off miR-198 expression in favor of sustained FSTL1 translation, driving metastasis through dual parallel pathways involving DIAPH1 and FSTL1. DIAPH1, a miR-198 target, enhances directional migration through sequestration of Arpin, a competitive inhibitor of Arp2/3 complex. FSTL1 blocks Wnt7a-mediated repression of extracellular signal–regulated kinase phosphorylation, enabling production of MMP9, which degrades the extracellular matrix and facilitates metastasis. The prognostic significance of the FSTL1-DIAPH1 gene pair makes it an attractive target for therapeutic intervention.
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Gao, Xueying, Ying Tang, and Yunping Ma. "Bone Marrow Mesenchymal Stem Cells (BMSCs)-Triggered Up-Regulation of miR-198 Impedes the Aggressive Migration and Invasion of Cervical Cancer Cells." Journal of Biomaterials and Tissue Engineering 12, no. 7 (July 1, 2022): 1285–92. http://dx.doi.org/10.1166/jbt.2022.3033.

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As a subset of RNAs without protein-coding function, short non-coding RNAs (microRNAs) are reported to contribute to the progress of multiple disorders. Nevertheless, the precise function of miR-198 in human cervical cancer is still an open question. RNA sequencing between cervical cancer cell lines and normal cervical epithelial cells identified CCAR1 to be highly expressed in cervical cancer. Cells were transfected with si-CCAR1 followed by analysis of cell behaviors using clonogenic assay and transwell migrating assay. The binding of miR-198 and CCAR1 was verified by a dual-luciferase reporter gene experiment. CCAR1 was highly expressed in cervical cancer tissues and cell lines and associated with tumor staging. Knockdown of CCAR1 restrained the malignant phenotypes of cervical cancer cells. CCAR1 was a target of miR198. Co-culture with BMSCs upregulated miR-198 expression, resulting in impediment of the aggressive phenotypes of cervical cancer cells, which was mediated by suppression of CCAR1 and release of inflammatory factors. In conclusion, CCAR1 level is increased in cervical cancer tissues or cell lines. Co-culture of BMSCs can facilitate the proliferating, migrating and invading activities of cervical cancer cells but reduce the release of inflammatory factors which is possibly through manipulating the axis of miR-198/CCAR1.
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Wu, Shujun, Hui Li, Chunya Lu, Furui Zhang, Huaqi Wang, Xinhua Lu, and Guojun Zhang. "Aberrant expression of hsa_circ_0025036 in lung adenocarcinoma and its potential roles in regulating cell proliferation and apoptosis." Biological Chemistry 399, no. 12 (November 27, 2018): 1457–67. http://dx.doi.org/10.1515/hsz-2018-0303.

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AbstractAs the most common histological subtype of lung cancer, lung adenocarcinoma remains a tremendous risk to public health, which requires ceaseless efforts to elucidate the potential diagnostic and therapeutic strategies. Circular RNAs (circRNAs) have been identified with emerging roles in tumorigenesis and development. Our preliminary work noticed that hsa_circ_0025036 was significantly upregulated in lung adenocarcinoma tissues. However, its specific roles in lung adenocarcinoma remain unclear. The results in this study revealed that hsa_circ_0025036 existed as a circular form and was aberrantly upregulated in lung adenocarcinoma tissues via quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Its expression level exhibited a close link with aggressive clinicopathological parameters including cancer differentiation, TNM stage and lymph node metastasis. hsa_circ_0025036 knockdown significantly suppressed cell proliferation and promoted cell apoptosis in A549 and Calu-3 cells. Moreover, hsa_circ_0025036/miR-198/SHMT1&TGF-αaxis was identified via bioinformatics analysis and Dual-Luciferase Reporter assays. miR-198 inhibitors reversed the function of hsa_circ_0025036 knockdown. hsa_circ_0025036 knockdown exerted similar effects with miR-198 upregulation on cell proliferation and apoptosis. In conclusion, we demonstrate that hsa_circ_0025036 regulates cell proliferation and apoptosis in lung adenocarcinoma cells probably via hsa_circ_0025036/miR-198/SHMT1&TGF-αaxis. hsa_circ_0025036 may serve as a potential prognostic biomarker and a therapeutic target for lung adenocarcinoma.
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LU, JIANXIN, BONNIE CHING-HA KWAN, FERNAND MAC-MOUNE LAI, LAI-SHAN TAM, EDMUND KWOK-MING LI, KAI-MING CHOW, GANG WANG, PHILIP KAM-TAO LI, and CHEUK-CHUN SZETO. "Glomerular and tubulointerstitial miR-638, miR-198 and miR-146a expression in lupus nephritis." Nephrology 17, no. 4 (April 17, 2012): 346–51. http://dx.doi.org/10.1111/j.1440-1797.2012.01573.x.

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Marín-Müller, Christian, Dali Li, Jian-Ming Lu, Zhengdong Liang, Osvaldo Vega-Martínez, William Fisher, Changyi Chen, and Qizhi Cathy Yao. "MiR-198 sensitizes pancreatic cancer to gemcitabine treatment through downregulation of VCP-mediated autophagy maturation." Journal of Clinical Oncology 40, no. 16_suppl (June 1, 2022): e16290-e16290. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.e16290.

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e16290 Background: The mechanism of human pancreatic ductal adenocarcinoma (PDAC) resistance to nucleoside analog and first-line chemotherapy drug gemcitabine is not clearly understood, but some studies have associated it with increased autophagy. In cancer biology, autophagy plays dual roles as it can promote tumor suppression during early stages, but in established tumors, it plays a crucial role in tumor growth by enhancing survival under metabolic and therapeutic stress. We have previously found that miR-198 acts as a tumor suppressor in PDAC through the targeting of a network of tumorigenic factors, including the Valosin-containing protein (VCP), which has been reported to play an important role in autophagy. In this study, we investigate whether the repression of VCP through miR-198 replacement disrupts the autophagy process and sensitizes PDAC cells to gemcitabine treatment. Methods: MIAPaCa2 cells with forced overexpression of mesothelin (MSLN) and AsPC-1 cell lines and, CDX and PDX mouse models were used for gemcitabine sensitization studies. For miR-198 replacement, a miR-198 expression vector-loaded lactic co-glycolic-acid-modified polyethylenimine polyplex (LPNP-p198) was used. Autophagy disruption experiments were run over miR-198 and/or VCP overexpressing cell lines. Nude mice were used for subcutaneous and orthotopic CDX models and SCID/Beige were used for the subcutaneous PDX model. Results: Cell lines were treated with LPNP-p198 in combination with gemcitabine and cell growth was significantly inhibited when compared to gemcitabine alone. Additionally, it was determined that miR-198 disrupts the autophagy maturation process and, that it is then restored by overexpression of VCP. LPNP-p198 can effectively enter tumor cells and induce tumor sensitization in vivo, resulting in an 80-90% reduction of tumor burden and metastatic spread in the LPNP-p198 plus gemcitabine group when compared to controls, with the concomitant downregulation of VCP expression in the tumor tissue. In addition, this group had the fewest mice with jaundice, ascites, and metastases to the abdominal cavity, spleen, liver, and kidney. Finally, to address the potential of the observed effect in the context of the heterogenic nature of PDAC, we confirmed our findings in a PDX mouse model, where a marked reduction in tumor burden was observed in the LPNP-p198 plus gemcitabine group compared to controls. Conclusions: Our findings indicate that miR-198 replacement disrupts the autophagy maturation process and sensitizes PDAC cells to gemcitabine through VCP repression, indicating a potential therapeutic strategy for targeting gemcitabine-resistant PDAC and, establishing the use of LPNPs as a prototype for effective nucleic acid delivery in vitro and in vivo, with potential to be used from bench to clinic.
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Marin-Muller, Christian, Dali Li, Jian-Ming Lü, Zhengdong Liang, Osvaldo Vega-Martínez, Sue E. Crawford, Mary K. Estes, William E. Fisher, Changyi Chen, and Qizhi Yao. "Nanoparticle-Mediated Therapy with miR-198 Sensitizes Pancreatic Cancer to Gemcitabine Treatment through Downregulation of VCP-Mediated Autophagy." Pharmaceutics 15, no. 8 (July 28, 2023): 2038. http://dx.doi.org/10.3390/pharmaceutics15082038.

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Pancreatic ductal adenocarcinoma (PDAC) remains an extremely aggressive disease characterized by rapidly acquired multi-drug resistance, including to first-line chemotherapeutic agent gemcitabine. Autophagy is a process that is often exploited by cancer and is one of several intrinsic factors associated with resistance to gemcitabine. We have previously found that miR-198 acts as a tumor suppressor in PDAC through the targeting of factors including Valosin-containing protein (VCP). VCP has been reported to play an important role in autophagic flux. In this study, we investigated whether the repression of VCP through miR-198 administration disrupts the autophagy process and sensitizes PDAC cells to gemcitabine treatment in vitro. Moreover, we used LGA-PEI (LPNP) nanoparticles to effectively administer miR-198 to tumors in vivo, inducing tumor sensitization to gemcitabine and leading to a significant reduction in tumor burden and metastases and a concomitant downregulation of VCP expression and autophagy maturation. Our results indicate a potential therapeutic strategy for targeting gemcitabine resistant PDAC and establishes the use of LPNPs for effective therapeutic delivery of nucleic acids in vitro and in vivo.
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Liu, Man, Yao Meng, Keren He, and Chonglin Luan. "Hsa_circ_0002060 Knockdown Ameliorates Osteoporosis by Targeting MiR-198-5p." Biological and Pharmaceutical Bulletin 44, no. 1 (January 1, 2021): 88–95. http://dx.doi.org/10.1248/bpb.b20-00643.

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Abhilasha, A., P. Mitra, S. Suri, I. Saxena, R. K. Shukla, and P. Sharma. "T133 Circulating levels of miR-24-3p and miR-198 in type 2 diabetes mellitus." Clinica Chimica Acta 530 (May 2022): S119. http://dx.doi.org/10.1016/j.cca.2022.04.612.

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Dissertations / Theses on the topic "MiR-198"

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Elfimova, Natalia [Verfasser]. "Die Rolle der Tumorsuppressor-miR-198 in der hepatozellulären Karzinogenese / Natalia Elfimova." Köln : Deutsche Zentralbibliothek für Medizin, 2013. http://d-nb.info/1046228315/34.

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Kaushik, Pankhuri. "Investigating the role of miR-198 in oral squamous cell carcinoma pathogenesis." Thesis, 2023. https://etd.iisc.ac.in/handle/2005/6197.

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Evidence supports the critical role of microRNA (miRNA) dysregulation in several diseases including cancers. The aberrant expression of numerous tumor suppressor and oncogenic miRNAs is a well-established driving factor in tumor progression. Though several mechanisms are reported to cause downregulation of tumor suppressor miRNAs, epigenetic silencing seems to play a major role. Pharmacological drugs are mostly employed for the reactivation and identification of epigenetically silenced tumor suppressor miRNAs. To this end in our laboratory, the miRNA microarray analysis of miRNA enriched RNA samples from OSCC SCC131 cells treated separately with DMSO (vehicle control) and 5-Azacytidine (a DNMT inhibitor) had previously revealed the upregulation and downregulation of 50 and 28 miRNAs respectively. In the present study, we have elucidated the role of miR-198 which is one of the miRNAs found to be upregulated following the 5-Azacytidine treatment. We confirmed the upregulation of miR-198 induced by 5-Azacytidine treatment using qRT-PCR and established its tumor suppressive function by checking its cell proliferating ability using trypan blue dye exclusion assay in OSCC cells from SCC084 and SCC131 cell lines. Since miRNAs bind to their target genes to bring about changes in gene expression, we wanted to identify a novel target gene for miR-198. Using bioinformatics and molecular approaches, we showed that miR-198 regulates the expression of the oncogene TOPORS at both the transcript and protein levels in OSCC cells in a dose-dependent manner. Using the dual-luciferase reporter assay, we also established the direct interaction of miR-198 with the 3’UTR of TOPORS in a sequence-specific manner. We hypothesised that miR-198 downregulation might be the cause of increased expression of TOPORS in OSCC and miR-198 might play a critical role in tumorigenesis. Thus, we analysed the expression of miR-198 and TOPORS in six different cancer cell lines and 39 matched normal oral tissue and OSCC patient samples and established the biological relevance of this interaction. We also showed that miR-198 suppressed the cell proliferation and anchorage-independent growth, and enhanced apoptosis of OSCC cells, in part, by targeting the 3’UTR of TOPORS. To elucidate the downstream effectors of miR-198 and TOPORS interaction, we analysed the p53/p21 signaling, and our results showed that miR-198 enhances this signaling pathway, in part, through the miR-198-TOPORS-p53-p21 axis. We also investigated the expression of TP53 (p53) and CDKN1A (p21) transcripts in our OSCC patient cohort and showed the clinical relevance of the p53-p21 pathway in these patients. To uncover the mechanism for upregulation of miR-198 following 5-Azacytidine, we identified an independent promoter for the MIR198 gene using the dual-luciferase reporter assay. We then analysed the methylation status of the MIR198 promoter in DMSO and 5-Azacytidine treated SCC131 cells, using bisulphite sequencing PCR. The results showed that the promoter methylation of MIR198 is responsible for its downregulation/silencing in SCC131 cells. We also showed that the promoter methylation of MIR198 causes differential miR-198 expression in MCF7 and MDA-MB-231 cells (breast cancer) and speculate the involvement of the same mechanism in other cancers. We also showed that the differential methylation pattern of the MIR198 promoter is inversely correlated with p21 levels in MCF7 and MDA-MB-231 cells, indicating the relevance of miR-198-TOPORS-p53-p21 axis in these cell lines. Taken together, our study suggests that miR-198 is epigenetically silenced by hypermethylation of the MIR198 promoter in OSCC, and exerts its tumor suppressive effect, in part, by regulating TOPORS, and the interaction between miR-198 and TOPORS is biologically relevant.
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Yi-TaTsai and 蔡易達. "The human hepatitis c virus (HCV) core protein has a role in modulating hsa-Let-7b, hsa-miR-122, hsa-miR-199 and hsa-miR-198." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/shtsrd.

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碩士
國立成功大學
分子醫學研究所
102
Summary The hepatitis C virus (HCV) core protein (HCVcore) constitutes the viral nucleocapsid structure, and is involved in viral persistence and pathogenesis possibly by interacting with host factors to modulate viral replication and cellular function. It is known that Dicer is an important component of microRNA processor, and HCVcore is associated with Dicer. These pieces of evidence suggest that HCVcore may modulate microRNA biogenesis or metabolism to regulate HCV infection and tumorigenesis. Because HCVcore may interact with many critical components of microRNA processing complexes, we ask in this study whether the levels of certain microRNAs (i.e., hsa-mir-122, hsa-let-7b, hsa-mir-199 and hsa-mir-198) would be affected by the presence of HCVcore in a Huh7.5 cell lines with replicating HCV. Firstly, we compared the 4 endogenous microRNA levels between Huh7.5 with or without replicating FGR (HCV full-genome replicon) by qPCR. The patterns of hsa-mir-122 and hsa-let-7b expression levels in cells with or without FGR are consistent with others in previous literatures, suggesting that our quantitation methods are reliable. Yet we first point out that HCV infection would increase expression of hsa-mir-199 and hsa-mir-198. Secondly, our result indicated that the structural proteins have roles in the modulation of endogenous microRNA. Finally, our result showed that the presence of HCVcore increases the expression level of hsa-mir-122, hsa-let-7b, hsa-mir-199 and hsa-mir-198. Collectively, our results indicated that HCVcore has an essential role in modulating microRNAs during HCV infection. Keyword: HCV, HCVcore, MicroRNA, hsa-miR-122, hsa-miR-198, hsa-miR-199, hsa-Let-7b
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Conference papers on the topic "MiR-198"

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Yu, X., H. Eischeid-Scholz, M. Schmiel, L. Wang, R. Büttner, and M. Odenthal. "MiR-198 overexpression leads to its vesicular release from hepatocellular carcinoma cells." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677242.

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Ogunwobi, Olorunseun O., Jian Li, Xiangxuan Zhao, Jose Trevino, Thomas George, and Chen Liu. "Abstract 896: miR-198 silencing is a mechanism of gemcitabine resistance in human pancreatic adenocarcinoma." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-896.

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Yu, X., H. Eischeid, M. Schmiel, R. Büttner, and M. Odenthal. "Overexpression of tumor suppressor miR-198 in hepatoma cells leads to its spontaneous and active export via vesicles." In 36. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3402225.

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Miyake, Keisuke, Takatsugu Ishimoto, Hidetaka Sugihara, Kojiro Eto, Daisuke Izumi, Junji Kurashige, Yukiharu Hiyoshi, et al. "Abstract 198: Helicobacter pylori infection via miR-328 suppression and CD44 expression in gastric mucosa causes gastric cancer initiation and progression." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-198.

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Han, Hye Sook, Jieun Yun, and Ok-Jun Lee. "Abstract 4165: Combination of cell-free miR-198, carcinoembryonic antigen, and CYFRA 21-1 as a diagnostic biomarker for lung adenocarcinoma-associated malignant pleural effusion." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4165.

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Murakami, Tomohiro, Hirotoshi Kikuchi, Hisahito Ishimatsu, Sanshiro Kawata, Amane Hirotsu, Tomohiro Matsumoto, Yusuke Ozaki, et al. "Abstract 1067: Tenascin C in colorectal cancer stroma is a predictive marker for liver metastasis and is a potent target of miR-198 as identified by microRNA analysis." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1067.

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