Anticancer function of alpha-solanine in lung adenocarcinoma cells by inducing microRNA-138 expression

作者：Zhang, Furui; Yang, Rui; Zhang, Guojun^*; Cheng, Ruirui; Bai, Yong; Zhao, Huasi; Lu, Xinhua; Li, Hui; Chen, Shanshan; Li, Juan; Wu, Shujun; Li, Ping; Chen, Xiaonan; Sun, Qianqian; Zhao, Guoqiang^*

来源：Tumor Biology, 2016, 37(5): 6437-6446.

DOI：10.1007/s13277-015-4528-2

• Lung adenocarcinoma cells
• alpha-Solanine
• MiR-138
• Migration
• Invasion
• Chemosensitivity
• Radiosensitivity

Currently, lung cancer is still a main cause of malignancy-associated death worldwide. Even though various methods for prevention and treatment of lung cancer have been improved in recent decades, the 5-year survival rate has remained very low. Insights into the anticancer function of small-molecule anticancer compounds have opened our visual field about cancer therapy. alpha-Solanine has been well studied for its antitumor properties, but its effect in lung cancer and associated molecular mechanisms have not yet been evaluated. To explore the anticancer function of alpha-solanine, we performed an MTT assay, Transwell arrays, colony-forming survival assay, quantitative reverse transcription PCR (qRT-PCR), Western blotting, and dual luciferase reporter assays in A549 and H1299 cells. We found that alpha-solanine not only inhibited cell migration and invasion ability but also enhanced the chemosensitivity and radiosensitivity of A549 and H1299 cells. Moreover, we discovered that alpha-solanine could affect the expression of miR-138 and focal adhesion kinase (FAK), both of which were also found to affect the chemosensitivity and radiosensitivity of A549 and H1299 cells. In conclusion, alpha-solanine could affect miR-138 and FAK expression to restrict cell migration and invasion and enhance the chemosensitivity and radiosensitivity of A549 and H1299 cells. The alpha-solanine/miR-138/FAK cascade can probably be a potential therapy target against lung adenocarcinoma.

• 出版日期2016-5
• 单位郑州大学