circPGAM1 enhances autophagy signaling during laryngocarcinoma drug resistance by regulating miR-376a

0301 basic medicine Mice, Inbred BALB C Mice, Nude Antineoplastic Agents Apoptosis RNA, Circular 3. Good health Gene Expression Regulation, Neoplastic MicroRNAs 03 medical and health sciences Drug Resistance, Neoplasm Cell Line, Tumor Autophagy Animals Humans Cisplatin Laryngeal Neoplasms
DOI: 10.1016/j.bbrc.2020.10.063 Publication Date: 2020-10-26T09:11:27Z
ABSTRACT
circRNAs have been shown to be involved in cancer progression. It is unclear whether circPGAM1 exerts its effect on laryngocarcinoma drug resistance. In this study, we employed colony formation and MTT assay to determine colony number and cell viability under cisplatin treatment. TUNEL experiment was used to evaluate apoptosis of laryngocarcinoma cells in the presence of cisplatin. Xenograft tumor experiment was performed to assess in vivo tumor growth of SNU46 cells. We found that circPGAM1 enhanced colony formation and viability of SNU46 and M4E cells. In contrast, circPGAM1 caused attenuated cell apoptosis. Furthermore, we also confirmed that circPGAM1 played a key role in tumor growth in animal model and clinical patients. miR-376a was identified and proved to act as key effector for circPGAM1-mediated drug resistance. Finally, autophagy-related gene ATG2A was shown to rescue miR-376a-modulated drug resistance of laryngocarcinoma cells. Herein, we illuminate the role of circPGAM1 in laryngocarcinoma drug resistance, thereby facilitating development of targeted therapy for treating laryngocarcinoma.
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