m6A-modified circFOXK2 targets GLUT1 to accelerate oral squamous cell carcinoma aerobic glycolysis

被引:30
作者
Cui, Yameng [1 ]
Liu, Jingwen [2 ]
Liu, Lina [3 ]
Ma, Xiaozhou [2 ]
Gui, Yu [2 ]
Liu, Hao [3 ]
Zhao, Wei [2 ]
机构
[1] Tianjin Med Univ, Dept Integrat Oncol, Canc Inst & Hosp, Tianjin 300060, Peoples R China
[2] Tianjin Med Univ, Sch & Hosp Stomatol, Tianjin 300070, Peoples R China
[3] NanKai Univ, Tianjin Stomatol Hosp, Hosp Stomatol, Dept Prosthodont, Tianjin 300041, Peoples R China
基金
中国国家自然科学基金;
关键词
D O I
10.1038/s41417-022-00526-6
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
N-6-methyladenosine (m(6)A) is an abundant nucleotide modification in mRNA, and its emerging roles have been gradually identified. However, the potential function of m(6)A and m(6)A-modified circular RNA (circRNA) is still unclear. Here, m(6)A-circRNA epitranscriptomic microarray analysis revealed a high-expressed m(6)A-modified circFOXK2 (hsa_circ_0000816, from FOXK2 gene) in oral squamous cell carcinoma (OSCC). For the biofunctions of OSCC, results revealed that circFOXK2 promoted the malignant phenotypes of OSCC cells. Methylated RNA immunoprecipitation sequencing (MeRIP-Seq) demonstrated that a remarkable m(6)A modified site was installed on glucose transporter 1 (GLUT1) mRNA. Mechanistically, circFOXK2 promoted the GLUT1 mRNA stability through cooperating with insulin-like growth factor 2 mRNA binding protein 3 (IGF2BP3) in a m(6)A-dependent manner. In summary, the present study explored the oncogenic role of m(6)A-modified circFOXK2 in OSCC through the m(6)A-dependent IGF2BP3/GLUT1 axis, indicating a potential therapeutic target for OSCC. [GRAPHICS] .
引用
收藏
页码:163 / 171
页数:9
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