Swertiamarin suppresses proliferation, migration, and invasion of hepatocellular carcinoma cells via negative regulation of FRAT1

Studies have shown that swertiamarin (STM) has multiple biological activities, but its antitumour effects and molecular mechanisms are still unclear. The present research aimed to validate the STM's impacts on the proliferation, migration, and invasion of hepatocellular carcinoma (HCC) cells, and to study its potential mechanism. Two HCC cell lines were treated with STM. Tumour growth was observed by the mouse tumour xenografts model. HCC cell lines stably expressing frequently rearranged in advanced T-cell lymphomas 1 (FRAT1) were generated by lentivirus-mediated overexpression. Cell viability, proliferation, migration, and invasion were observed using Cell Counting Kit-8 (CCK8), the xCELLigence Real-Time Cell Analyzer system (RTCA), and transwell analysis, respectively. Quantitative real-time polymerise chain reaction (qRT-PCR) and Western blotting were used to observe the expression of FRAT1 and proteins related to the Wnt/P-catenin signalling pathway. Tumour growth was inhibited by STM in vivo. STM suppressed the proliferation, migration, and invasion of HCC cells. STM negatively regulated FRAT1 expression, whereas overexpressed FRAT1 blocked the antitumour function of STM. The results revealed that STM suppressed the FRAT1/Wnt/beta-catenin signalling pathway. The findings of this study provide new insights into investigation of therapeutic strategies against HCC.