Silibinin reduces cell proliferation and migration via EMT pathway in TFK-1 cell line

Abstract Objectives Cholangiocarcinoma (CCA) is usually diagnosed at a late stage due to resistance to chemotherapeutic drugs. Epithelial mesenchymal transition (EMT) is a biological process in cancer that allows multiple biochemical changes that enable epithelial cells to acquire a mesenchymal phenotype. In the present study, we focused on the EMT process which is an important in carcinogenesis and metastatic progression, and also investigate the effect of silibinin on cell proliferation, colony formation, migration, apoptosis, cell cycle and EMT. Methods Cell viability, apoptosis and cell cycle were measured by Muse Cell Analyzer. All the protein levels were determined by ELISA method. Results We found that silibinin significantly reduced cell proliferation in a dose-dependent manner and the IC50 value was 200 μM. Silibinin, significantly inhibited colony formation, inhibited cell migration of cancer cells induced total apoptosis due to the induction of early and late apoptosis, arrest cancer cells in the G0/G1 phase of the cell cycle compared to the control group. We found that E-cadherin, N-cadherin, Vimentin and α-SMA protein levels were significantly decreased in the silibinin group compared to the control group. Conclusions Our results showed that silibinin could significantly prevent tumor proliferation, reduce colony formation, prevent migration, increase the arrest of the G0/G1 phase and induce apoptosis progress in human extracellular cholangiocarcinoma cell line. Another important data is that silibinin inhibits EMT in the cholangiocarcinoma cell line (TFK-1). Our study shows significant effects of silibinin in the TFK-1 cell line, which may be exciting to explore its implications in future animal studies.