Research Paper Volume 13, Issue 6 pp 8078—8094
Flotillin-2 promotes cell proliferation via activating the c-Myc/BCAT1 axis by suppressing miR-33b-5p in nasopharyngeal carcinoma
- 1 Department of Otolaryngology Head and Neck Surgery, Xiangya Hospital, Central South University, Changsha 410008, China
- 2 College of Biology and Environmental Sciences, Jishou University, Jishou 416000, China
- 3 Department of Pathology, Changsha Central Hospital, Changsha 410004, China
- 4 Research Center of Carcinogenesis and Targeted Therapy, Xiangya Hospital, Central South University, Changsha 410008, China
- 5 Department of Histology and Embryology, School of Basic Medicine, Central South University, Changsha 410013, China
Received: November 23, 2020 Accepted: February 9, 2021 Published: March 19, 2021https://doi.org/10.18632/aging.202726
How to Cite
Copyright: © 2021 Liu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Previously, we elucidated the function of flotilin-2 (FLOT2) and branched-chain amino acid transaminase 1(BCAT1) in nasopharyngeal carcinoma (NPC). However, the relationship between FLOT2 and BCAT1 in promoting NPC progression remains unknown. Here, we observed that FLOT2 upregulated BCAT1 expression in NPC cells. Ectopic expression of BCAT1 significantly antagonized the inhibitory effects on NPC cell proliferation induced by FLOT2 depletion. Consequently, BCAT1 knockdown markedly inhibited the pro-proliferative effects of FLOT2 overexpression in NPC cells. FLOT2 expression was positively correlated with BCAT1 expression in NPC tissues and was inversely correlated with the prognosis of NPC patients. Mechanistically, FLOT2 maintains the expression level of c-Myc, a positive transcription factor of BCAT1, and subsequently promote BCAT1 transcription. FLOT2 inhibited miR-33b-5p in NPC cells and attenuated its inhibitory effects on c-Myc. Further, experimental validation of the function of the FLOT2/miR-33b-5p/c-Myc/BCAT1 axis in regulating NPC cell proliferation was performed. Our results revealed that FLOT2 promotes NPC cell proliferation by suppressing miR-33b-5p, to maintain proper levels of c-Myc, and upregulate BCAT1trancription. Therefore, the FLOT2/miR-33b-5p/c-Myc/BCAT1 axis is a potential therapeutic target for NPC.