Implications of TRAP1 modulate cell invasion and epithelial–mesenchymal transition in liver cancer: evidence from in vitro HepG2 study

Abstract

Abstract Background: Although the list of biomarkers is still growing, the molecular mechanisms associated with liver cancer development and progress are still uncertain. We recently confirmed the high expression of molecular chaperone TRAP1 in HepG2 cells. In this context, the aim of this study is to investigate the effects of gain or loss function of TRAP1 on cell invasion in HepG2 cells, and to evaluate whether TRAP1 regulate cell invasion by controlling EMT related gene expression. Methods: The TRAP1 overexpression and knockdown HepG2 cells were constructed by lentivirus method. To investigate the effects of TRAP1 on cell function, cell proliferation was measured by MTT method. Cell apoptosis was detected by flow cytometry. The migration and invasion ability were measured by wound healing assay and transwell migration assay. mRNA and protein expression of TRAP1 and EMT related genes were performed by qRT-PCR and western blot, respectively. Results: TRAP1 overexpression and knockdown cells were successfully established in two recombined cell lines, we studied the general effects of TRAP1 and its association to EMT pathway. The results indicated that TRAP1 promoted cell malignant phenotypes, which including cell proliferation, apoptosis and migration. Besides, TRAP1 inhibited the epithelial markers expression and increased mesenchymal markers expression in both mRNA and protein levels. Conclusions: These results may provide novel approaches in liver cancer with increasing TRAP1 expression, which could be associated with EMT pathway, with potential future intervention in liver cancer invasion and metastasis.