Sinomenine inhibits human lung cancer A549 cell invasionby mediating STAT3 signaling pathway

• 作 者: Shulong Jiang Baojin Hua Yebo Gao Wei Hou Rui Liu Xin Qi Xia Xu Jie Li Yanju Bao Honggang Zheng
• 机 构: DepartmentofOncology,JiningFirstPeople'sHospital,Shandong,China;DepartmentofOncology,Guang'anmenHo
• 出 处: 2015年全国中医肿瘤学术年会暨第三届岐黄论坛分论坛
• 发表日期: 2015年7期
• 关键词: Sinomenine STAT3 Epithelial-mesenchymal transition Lung cancer cell invasion

　　Cumulated date suggest that the failure of lung cancer treatment aremainly due to tumor invasion and metastasis.STAT3, an EMT-inducing transcription factor, is a key signaling molecule involved in the proliferation, apoptosis, invasion, andmetastasis of tumors.Sinomenine is an alkaloid compound with an anti-neoplastic potential against a variety of cancer cells.The purpose of this study was to assess the antitumor mechanisms of sinomenine in human lung cancer A549 cells.The results showed that sinomenine manifested dose-dependent cytotoxicity and induction of apoptosis.The protein expression of JAK2, STAT3, p-STAT3, SNAIL, N-cadherin, and Vimentin were all decreased, while E-cadherin protein expression was increased in sinomenine-treated cells.Sinomenine regulation of STAT3, N-cadherin, and E-cadherin were further confirmed by quantitative RT-PCR and immunofluorescent staining assays.We demonstrated that sinomenine exerts inhibitory effects on human lung cancer A549 cell invasion, possibly via the inhibition of STAT3 signaling.These findings provide a novel insight into the role of sinomenine in the treatment of non-small cell lung cancer.