Paclitaxel exerts anticancer bioactivity on SGC 7901 human gastric adenocarcinoma cell line through inhibition of Akt / mTOR signaling pathway

Gastric cancer is one of the most prevalent malignancies and the leading cause of cancer mortality. Paclitaxel, a traditional medicine, is originally extracted from pacific yew tree. It has been reported that paclitaxel can treat multiple human malignancies including gastric cancer. However, the underlying mechanism has not been fully understood. In our study, SGC-7901 human gastric adenocarcinoma cell line was cultured and treated with paclitaxel. Cell Counting Kit-8 (CCK-8) and colony formation assay were performed to examine cell viability. Cell migration and metastasis ability were measured by cell invasion assay. Moreover, cell cycle was determined by the Flow Cytometry, Hoechst33342/PI (propidium iodide) double staining and Flow Cytometry were both employed to test cell apoptosis. To further explore the underlying mechanisms of paclitaxel in gastric cancer, western blotting was performed to detect the protein expression of phospho-Akt (p-Akt) and phospho-mTOR (p-mTOR). Our results showed that paclitaxel obviously reduced SGC-7901 cell viability and cellular colony formation ratio compared with the control (P<0.01). Meanwhile, paclitaxel effectively inhibited cell migration and metastasis, the number of invaded cells reduced significantly (P<0.01). Flow Cytometry and Hoechst/PI double staining results also showed paclitaxel induced SGC-7901 cell apoptosis (P<0.01) and let cell cycle arrest at G2/M phase. Furthermore, paclitaxel strongly decreased the expression of p-Akt and p-mTOR proteins. Collectively, our study indicated that paclitaxel exerts an obvious anticancer bioactivity on SGC-7901 human gastric adenocarcinoma cell line, which is possibly, mediated through inhibition of Akt/mTOR signaling pathway.