Molecular mechanism of the signaling axis regulating the progression of hepatocellular carcinoma.

BACKGROUND

To investigate the roles of and its potential mechanisms in hepatocellular carcinoma (HCC).

METHODS

The functions of were identified and measured by MTT [3-(4,5)-dimethylthiahiazo(-z-y1)-3,5-di-phenytetrazoliumromide], colony formation, transwell, and flow cytometry assays. A luciferase assay was applied to verify the direct binding of on 3'untranslated region (3'UTR). An experiment was then used to investigate the biological effects of and . A co-immunoprecipitation (COIP) assay was used to detect the protein interaction between and .

RESULTS

We found that overexpression suppressed cell proliferation, migration, and invasion in HCC. was also demonstrated as a direct target gene of miR-7. This study showed that could partially rescue the inhibitory effect of on the proliferation, migration, and invasion of HCC cells. Our research showed that could inhibit the epithelial-mesenchymal transition (EMT) pathway by regulating . We also further confirmed that inhibits the proliferation, migration, and invasion of Hep3B and Huh7 cells by targeting . Furthermore, we observed that the protein interacts with the protein and affects the development of liver cancer through . We also found that could promote the invasion and migration of liver cancer cells through inhibition. also inhibited the expression of Caspase 3/7 in hepatoma cells by inhibiting the expression of .

CONCLUSIONS

Our study demonstrated that may serve as a regulatory molecular axis for HCC treatment. Our results suggest that may have predictive value and represent a new treatment strategy for liver cancer.