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| Anti-tumor efficiency of α-solanine against nasopharyngeal carcinoma in vitro via ROS/mitochondrial pathway and its molecular mechanism |
| WU Xianmin, ZHANG Jie, YANG Zifei, YE Fan, ZHANG Yue, CHEN Xiaoyun |
| Department of Otolaryngology-Head and Neck Surgery, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325015, China |
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| Cite this article: |
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WU Xianmin,ZHANG Jie,YANG Zifei, et al. Anti-tumor efficiency of α-solanine against nasopharyngeal carcinoma in vitro via ROS/mitochondrial pathway and its molecular mechanism[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2021, 51(2): 87-92.
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Abstract Objective: To explore the effect of α-solanine on human nasopharyngeal carcinoma cell CNE-2 and its potential mechanism in vitro. Methods: CCK-8 assay was used to determine CNE-2 cell proliferation after α-solanine treatment. Flow cytometry was performed to detect cell apoptosis. Real-time PCR and Western blot were used to detect the expression level of apoptosis related genes in CNE-2 cells. Mito-SOX was used to analyze changes of ROS production level. The ultrastructure of mitochondria was observed under transmission electron microscope. Results: α-Solanine significantly inhibited cell activity and triggered cell apoptosis in a time- and dose-dependent manner. The expression of Aif and Caspase-8 was significantly increased in CNE-2 cells after 10 μmol/L α-solanine treatment of 48 h, compared with the control (P<0.01). The Bcl-2 expression and the Bcl-2/Bax ratio were significantly decreased after α-solanine treatment (P<0.05). α-Solanine significantly increased intracellular ROS levels. Transmission electron microscopy (TEM) showed mitochondrial damage in CNE-2 cells. Conclusion: α-Solanine can inhibit cell proliferation activity, induce increased ROS levels, cause mitochondrial damage, and finally trigger CNE-2 cell apoptosis through the mitochondrial pathway.
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Received: 21 September 2020
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