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m 6 A transferase METTL3‐induced lncRNA ABHD11‐AS1 promotes the Warburg effect of non‐small‐cell lung cancer
Author(s) -
Xue Lei,
Li Jun,
Lin Yihui,
Liu Degang,
Yang Qiang,
Jian Jinting,
Peng Jiangzhou
Publication year - 2021
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.30023
Subject(s) - carcinogenesis , cancer research , ectopic expression , downregulation and upregulation , biology , lung cancer , methyltransferase , long non coding rna , rna , warburg effect , cell growth , immunoprecipitation , cancer , microbiology and biotechnology , cancer cell , oncology , cell culture , genetics , medicine , gene , methylation
Abstract N 6 ‐methyladenosine (m 6 A) and long noncoding RNAs (lncRNAs) are both crucial regulators in non‐small‐cell lung cancer (NSCLC) tumorigenesis. However, the pathological roles of m 6 A and lncRNAs in NSCLC progression are still limited and undefined. Here, lncRNA ABHD11‐AS1 was upregulated in NSCLC tissue specimens and cells and the ectopic overexpression was closely correlated with unfavorable prognosis of NSCLC patients. Functionally, ABHD11‐AS1 promoted the proliferation and Warburg effect of NSCLC. Mechanistically, m 6 A profile was analyzed by methylated RNA immunoprecipitation sequencing (MeRIP‐Seq). MeRIP‐Seq presented that there was m 6 A modification site in ABHD11‐AS1. m 6 A methyltransferase‐like 3 (METTL3) installed the m 6 A modification and enhanced ABHD11‐AS1 transcript stability to increase its expression. In conclusion, our findings highlight the function and mechanism of METTL3‐induced ABHD11‐AS1 in NSCLC and inspire the understanding of m 6 A and lncRNA in cancer biology.