Abstract

Objective: We aimed to discuss the molecular mechanism of miR-378 in enhancing the invasion and migration of hepatoma carcinoma cells through targeted PTEN-based EMT regulation. Method: The human hepatoma cell line HepG2 was cultured. Cells in the logarithmic phase were collected and transfected using miR-378 mimics through liposome-mediated transfection method. Successfully transfected cells and the primary cancer cells were denoted as groups A and B. Each group had eight repeated holes. The invasion and migration abilities of both groups were tested by Transwell and wound-healing experiments at 24 and 48 h. The relative miR-378 mRNA expression levels of both groups were detected by reverse transcription-polymerase chain reaction. PTEN and EMT related proteins were tested by Western blot at 48 h. Differences between two groups were analysed by SPSS20.0. Results: The cell-leaching and wound-healing rates of group A at 24 and 48 h were lower than those of group B. Cell-leaching and wound-healing rates at 48 h were higher than those at 24 h. Differences were statistically significant (P<0.05). The relative expression levels of miR-378 mRNA and PTEN protein content of group A were significantly higher than those of group B, whereas relative expression levels of Protein Kinase B (PKB), Ki67 and Phosphatidylinositol 3 (PI3K) were significantly lower (P<0.05). Conclusions: Low expression of miR-378 was observed in hepatoma carcinoma cells, which can downregulates the expression of PTEN protein and upregulates the expression of EMT-related proteins, thereby enhancing their invasion and migration abilities.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.