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MicroRNA-15a inhibits hepatic stellate cell activation and proliferation via targeting SRY-box transcription factor 9
Accumulating research have indicated that microRNAs are associated with the progression of hepatic fibrosis (HF). Nevertheless, the biological role and function of microRNA (miR)-15a in HF are still unknown. Our data revealed that miR-15a expression was decreased in TGF-β1-treated LX-2 cells and CCl...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Taylor & Francis
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9276033/ https://www.ncbi.nlm.nih.gov/pubmed/35611752 http://dx.doi.org/10.1080/21655979.2022.2068895 |
Sumario: | Accumulating research have indicated that microRNAs are associated with the progression of hepatic fibrosis (HF). Nevertheless, the biological role and function of microRNA (miR)-15a in HF are still unknown. Our data revealed that miR-15a expression was decreased in TGF-β1-treated LX-2 cells and CCl(4)-induced mouse model. Additionally, miR-15a could directly target the 3’‑untranslated region of SRY-box transcription factor 9 (SOX9) to inhibit its expression. miR-15a overexpression attenuated the viability and invasion, but enhanced apoptosis in LX-2 cells. However, miR-15a knockdown had the opposite effects. Interestingly, SOX9 overexpression reversed the changes in cell viability, invasion and apoptosis mediated by miR-15a overexpression. Moreover, the miR-15a overexpression-mediated collagen I and alpha smooth muscle actin (a-SMA) downregulation were reversed by SOX9 overexpression. Overall, miR-15a could inhibit LX-2 cell viability and HF pathogenesis by targeting SOX9 in vitro and in vivo. |
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