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The m6A methyltransferase METTL3 contributes to Transforming Growth Factor-beta-induced epithelial-mesenchymal transition of lung cancer cells through the regulation of JUNB.

Biochem. Biophys. Res. Commun.2020 Mar 26;524(1):150-155. Epub 2020 Jan 22
Sasithorn Wanna-Udom 1 , Minoru Terashima 1 , Hanbing Lyu 1 , Akihiko Ishimura 1 , Takahisa Takino 2 , Matomo Sakari 3 , Toshifumi Tsukahara 3 , Takeshi Suzuki 4
Sasithorn Wanna-Udom 1 , Minoru Terashima 1 , Hanbing Lyu 1 , Akihiko Ishimura 1 , Takahisa Takino 2 , Matomo Sakari 3 , Toshifumi Tsukahara 3 , Takeshi Suzuki 4
+ et al

[No authors listed]

Author information
  • 1 Division of Functional Genomics, Cancer Research Institute, Kanazawa University, Kakuma-machi, Kanazawa, 920-1192, Ishikawa, Japan.
  • 2 Division of Education for Global Standard, Institute of Liberal Arts and Science, Kanazawa University, Kakuma-machi, Kanazawa, 920-1192, Ishikawa, Japan.
  • 3 Area of Bioscience and Biotechnology, Japan Advanced Institute of Science and Technology, Nomi, 923-1292, Ishikawa, Japan.
  • 4 Division of Functional Genomics, Cancer Research Institute, Kanazawa University, Kakuma-machi, Kanazawa, 920-1192, Ishikawa, Japan. Electronic address: suzuki-t@staff.kanazawa-u.ac.jp.

摘要


N6-Methyladenosine (m6A) is the most common internal chemical modification of mRNAs involved in many pathological processes including various cancers. In this study, we investigated the role of m6A methyltransferase METTL3 in TGF-β-induced epithelial-mesenchymal transition (EMT) of lung cancer cell lines. The expression of METTL3 and m6A RNA modification were increased during TGF-β-induced EMT of A549 and LC2/ad lung cancer cells. Knockdown of METTL3 inhibited TGF-β-induced morphological conversion of the cells, enhanced cell migration potential and the expression changes of EMT-related marker genes such as CDH1/E-cadherin, FN1/Fibronectin and VIM/Vimentin. Mechanistic investigations revealed that METTL3 knockdown decreased the m6A modification, total mRNA level and mRNA stability of JUNB, one of the important transcriptional regulators of EMT. Over-expression of JUNB partially rescued the inhibitory effects of METTL3 knockdown in the EMT phenotypes. This study demonstrates that m6A methyltransferase METTL3 is indispensable for TGF-β-induced EMT of lung cancer cells through the regulation of JUNB.

KEYWORDS: Epithelial-mesenchymal transition, JUNB, Lung cancer, METTL3, RNA methylation