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World J Surg Oncol ; 20(1): 175, 2022 Jun 02.
Artigo em Inglês | MEDLINE | ID: mdl-35655254

RESUMO

PURPOSE: This study aimed at investigating miR-382-5p expression in tissues and cell lines with hepatocellular carcinoma (HCC), its effects on the invasion of HCC cells, and related mechanisms. METHODS: miR-382-5p expression in HCC tissues, adjacent tissues, cell lines of normal hepatic cells, and HCC cells were detected by qRT-PCR, indicating its upregulation or downregulation in HCC cell lines (Hep3B and HCCLM3). The effect of miR-382-5p on cell invasion was observed by the Transwell experiment. The targeting relationship of miR-382-5p and the phosphatase and tensin homolog (PTEN) was analyzed using bioinformatics tools and the luciferase reporter gene assay. The correlation between miR-382-5p and PTEN was analyzed with Spearman correlation analysis. PTEN expression was observed after upregulation and downregulation of miR-382-5p expression. The effect of miR-382-5p on the expression of key proteins in PI3K/Akt signaling pathway was determined by Western blot. RESULTS: miR-382-5p expression was upregulated in both HCC tissues and cell lines (both P<0.05). Upregulation or downregulation of miR-382-5p significantly promoted or inhibited the invasion of cell lines, Hep3B, and HCCLM3. The luciferase reporter gene assay confirmed that PTEN is a target of miR-382-5p. The expressions of miR-382-5p and PTEN were negatively correlated (r=-0.742, P<0.001). Upregulation of PTEN expression by plasmid transfection can reverse the invasive effect of miR-382-5p on HCC cells. Upregulation of miR-382-5p can activate PI3K/Akt signaling pathway, and downregulation of miR-382-5p can inhibit PI3K/Akt signaling pathway. CONCLUSIONS: miR-382-5p can activate the PI3K/Akt signaling pathway by targeting PTEN and promote HCC cell invasion.


Assuntos
Carcinoma Hepatocelular , Neoplasias Hepáticas , MicroRNAs , Carcinoma Hepatocelular/patologia , Linhagem Celular Tumoral , Proliferação de Células/genética , Humanos , Neoplasias Hepáticas/patologia , Luciferases/metabolismo , MicroRNAs/genética , MicroRNAs/metabolismo , PTEN Fosfo-Hidrolase/genética , PTEN Fosfo-Hidrolase/metabolismo , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Transdução de Sinais
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