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.