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MicroRNA-3651 promotes the growth and invasion of hepatocellular carcinoma cells by targeting PTEN
BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in human worldwide. Evidence indicated that upregulation of microRNA-3651 (miR-3651) was observed in human HCC tissues. In this study, we explored the mechanisms by which miR-3651 regulated the proliferation, apopt...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6718252/ https://www.ncbi.nlm.nih.gov/pubmed/31695418 http://dx.doi.org/10.2147/OTT.S213705 |
Sumario: | BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in human worldwide. Evidence indicated that upregulation of microRNA-3651 (miR-3651) was observed in human HCC tissues. In this study, we explored the mechanisms by which miR-3651 regulated the proliferation, apoptosis and invasion of HCC. METHODS: The levels of miR-3651 in human HCC tissues were detected using qRT-PCR assay. In addition, transwell invasion and Western blot assay were conducted to detect cell invasion and apoptosis, respectively. Meanwhile, the dual-luciferase reporter assay was used to explore the interaction of miR-3651 and phosphate and tension homology deleted on chromsome ten (PTEN) in HCC. RESULTS: The levels of miR-3651 were upregulated in HCC tissues in comparison with the matched normal tissues. Overexpression of miR-3651 significantly promoted the proliferation and invasion of Huh-7 cells. In contrast, inhibition of miR-3651 markedly inhibited the proliferation and invasion of Huh-7 cells via promoting apoptosis. Moreover, downregulation of miR-3651 markedly inhibited tumor growth in vivo. Furthermore, bioinformatics analysis and luciferase reporter assay identified that PTEN was the directly binding target of miR-3651 in Huh-7 cells. Meanwhile, overexpression of miR-3651 obviously decreased the level of PTEN, and increased the expressions of p-p85 and p-Akt in Huh-7 cells. CONCLUSION: These results indicated that miR-3651 might act as a potential oncogene in HCC by targeting PTEN. Therefore, miR-3651 might be a novel therapeutic target for the treatment of HCC. |
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