Trichosanthin inhibits the proliferation of cervical cancer cells and downregulates STAT-5/C-myc signaling pathway

Abstract

BackgroundPrevious studies have indicated that Trichosanthin (TCS) exerts anti-virus, immunoregulation and a broad spectrum anti-tumor pharmacological activities. Trichosanthin is a promising agent for the treatment of cervical cancer. However, the exact effects and potential mechanism of TCS on cervical cancer are not well known. MethodThe cell viability of TCS on cervical cancer cell lines (HeLa and caski cells) were detected by a Cell Counting Kit-8 (CCK-8) assay. Cell proliferation was measured by Ki-67 staining and cell apoptosis was detected by flow cytometry. Cell migration and invasion were detected by wound assay and transwell assay, respectively. The levels of E-cadherin, N-cadherin, Snail, Bcl-2, Caspase-3, p-STAT5, STAT5, p-C-myc, C-myc were detected by western blot. ResultsThe present study showed that TCS inhibited the proliferation of HeLa and caski cells and reduced Ki-67 and P-C-myc expression. In addition, flow cytometric analysis showed that TCS induced the apoptosis of HeLa and caski cells. The potent effect of TCS on cell apoptosis as determined by the increase the levels of caspase-3 and decrease the levels of Bcl-2. TCS also inhibited cervical cancer cell invasion, migration and epithelial-mesenchymal transition (EMT). Furthermore, TCS treatment markedly inhibited the activation of STAT5/C-myc signaling pathway. ConclusionIn conclusion, the present study suggest that TCS inhibits the proliferation, migration and EMT of human cervical cancer cells, which maybe mediated by inhibiting the activation of STAT5/C-myc signaling pathway.