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2. METTL3-induced DLGAP1-AS2 promotes non-small cell lung cancer tumorigenesis through m6A/c-Myc-dependent aerobic glycolysis.

Author

Zhang, Qiang, Zhang, Yu, Chen, Hui, Sun, Lei-Na, Zhang, Bin, Yue, Dong-Sheng, Wang, Chang-Li, and Zhang, Zhen-Fa

Subjects
NON-small-cell lung carcinoma, GLYCOLYSIS, LINCRNA, ANTISENSE RNA, NEOPLASTIC cell transformation
Abstract

The critical roles of N6-methyladenosine (m6A) modification have been demonstrated by more and more evidence. However, the cross talk of m6A and long noncoding RNAs (lncRNAs) in non-small cell lung cancer (NSCLC) tumorigenesis is still unclear. Here, this work focused on the functions and molecular mechanism of m6A-modified lncRNA DLGAP1 antisense RNA 2 (DLGAP1-AS2) in NSCLC. Microarray analysis found that lncRNA DLGAP1-AS2 is upregulated in NSCLC cells. Clinical data showed that DLGAP1-AS2 high-expression was correlated with advanced pathological stage and poor prognosis. Functionally, DLGAP1-AS2 overexpression promoted the aerobic glycolysis and DLGAP1-AS2 knockdown suppressed the tumor growth of NSCLC cells. Mechanistically, m6A methyltransferase METTL3 enhanced the stability of DLGAP1-AS2 via m6A site binding. Moreover, DLGAP1-AS2 interacted with YTHDF1 to enhance the stability of c-Myc mRNA through DLGAP1-AS2/YTHDF1/m6A/c-Myc mRNA. In conclusion, our work indicates the functions of m6A-modified DLGAP1-AS2 in the NSCLC aerobic glycolysis, disclosing a potential m6A-dependent manner for NSCLC treatment. [ABSTRACT FROM AUTHOR]

Published
2022
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6. METTL3-induced DLGAP1-AS2 promotes non-small cell lung cancer tumorigenesis through m 6 A/c-Myc-dependent aerobic glycolysis.

Author

Zhang Q, Zhang Y, Chen H, Sun LN, Zhang B, Yue DS, Wang CL, and Zhang ZF

Subjects
Humans, Gene Expression Regulation, Neoplastic, Cell Proliferation genetics, Carcinogenesis genetics, Cell Transformation, Neoplastic genetics, RNA, Messenger metabolism, Glycolysis genetics, Cell Line, Tumor, Methyltransferases genetics, Methyltransferases metabolism, Carcinoma, Non-Small-Cell Lung pathology, RNA, Long Noncoding genetics, RNA, Long Noncoding metabolism, Lung Neoplasms pathology
Abstract

The critical roles of N 6 -methyladenosine (m 6 A) modification have been demonstrated by more and more evidence. However, the cross talk of m 6 A and long noncoding RNAs (lncRNAs) in non-small cell lung cancer (NSCLC) tumorigenesis is still unclear. Here, this work focused on the functions and molecular mechanism of m 6 A-modified lncRNA DLGAP1 antisense RNA 2 (DLGAP1-AS2) in NSCLC. Microarray analysis found that lncRNA DLGAP1-AS2 is upregulated in NSCLC cells. Clinical data showed that DLGAP1-AS2 high-expression was correlated with advanced pathological stage and poor prognosis. Functionally, DLGAP1-AS2 overexpression promoted the aerobic glycolysis and DLGAP1-AS2 knockdown suppressed the tumor growth of NSCLC cells. Mechanistically, m 6 A methyltransferase METTL3 enhanced the stability of DLGAP1-AS2 via m 6 A site binding. Moreover, DLGAP1-AS2 interacted with YTHDF1 to enhance the stability of c-Myc mRNA through DLGAP1-AS2/YTHDF1/m 6 A/c-Myc mRNA. In conclusion, our work indicates the functions of m 6 A-modified DLGAP1-AS2 in the NSCLC aerobic glycolysis, disclosing a potential m 6 A-dependent manner for NSCLC treatment.

Published
2022
Full Text
View/download PDF

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