Published on Jan. 5, 2020 in Gene volume 722DP - 2020 Jan 5TI - N6-methyladenosine METTL3 promotes the breast cancer progression via targetingBcl-2.PG - 144076LID - S0378-1119(19)30735-8 [pii]LID - 10.1016/j.gene.2019.144076 [doi]AB - N6-methyladenosine (m6A) is the most prevalent internal modification in mammalianmRNAs and methyltransferase-like 3 (METTL3) is a vital methyltransferase in m6Amodification. Here, this study tries to discover the regulatory role of METTL3 andits mechanism in the breast cancer tumorigenesis. Results found that METTL3 wasup-regulated in the breast cancer tissue and cells. In vivo and vitro, METTL3knockdown could decrease the methylation level, reduce the proliferation, acceleratethe apoptosis and inhibited the tumor growth. Moreover, we found that Bcl-2 acted asthe target of METTL3, thereby regulating the proliferation and apoptosis of breastcancer. This study could reveal the potential mechanism of m6A modification in thebreast cancer tumorigenesis, providing potential drug targets in the treatment.CI - Copyright © 2019 Elsevier B.V. All rights reserved.FAU - Wang, HongAU - Wang HAD - Breast Surgery Medicine, Zhong-Shan Hospital Affiliated with Fudan University,Shanghai 200032, China.FAU - Xu, BeiAU - Xu BAD - Internal Medicine-Oncology, Zhong-Shan Hospital Affiliated with Fudan University,Shanghai 200032, China.FAU - Shi, JunAU - Shi JAD - Department of Obstetrics and Gynecology, Renji Hospital, School of Medicine,Shanghai Jiao Tong University, Shanghai 200127, China. Electronic address:shijunrenji@yeah.net.LA - engPT - Journal ArticleDEP - 20190824PL - NetherlandsTA - GeneJT - GeneJID - 7706761RN - 0 (Proto-Oncogene Proteins c-bcl-2)RN - 1867-73-8 (N6-methyladenosine (m6A))RN - EC 2.1.1.- (Methyltransferases)RN - EC 2.1.1.62 (METTL3 protein, human)RN - K72T3FS567 (Adenosine)SB - IMMH - Adenosine/analogs &amp; derivatives/metabolismMH - ApoptosisMH - Breast Neoplasms/*enzymology/genetics/pathologyMH - Cell Line, TumorMH - Cell ProliferationMH - Disease ProgressionMH - FemaleMH - HumansMH - Methyltransferases/genetics/*metabolismMH - Proto-Oncogene Proteins c-bcl-2/*genetics/metabolismOTO - NOTNLMOT - Bcl-2OT - Breast cancerOT - METTL3OT - N6-methyladenosineOT - m6AEDAT- 2019/08/28 06:00MHDA- 2019/11/09 06:00CRDT- 2019/08/28 06:00PHST- 2019/06/15 00:00 [received]PHST- 2019/08/21 00:00 [revised]PHST- 2019/08/22 00:00 [accepted]PHST- 2019/08/28 06:00 [pubmed]PHST- 2019/11/09 06:00 [medline]PHST- 2019/08/28 06:00 [entrez]AID - S0378-1119(19)30735-8 [pii]AID - 10.1016/j.gene.2019.144076 [doi]PST - ppublishSO - Gene. 2020 Jan 5;722:144076. doi: 10.1016/j.gene.2019.144076. Epub 2019 Aug 24.</pre></div></body></html>().

PubMed ID: 31454538

DOI: S0378-1119(19)30735-8


Abstract:

N6-methyladenosine (m6A) is the most prevalent internal modification in mammalianmRNAs and methyltransferase-like 3 (METTL3) is a vital methyltransferase in m6Amodification. Here, this study tries to discover the regulatory role of METTL3 andits mechanism in the breast cancer tumorigenesis. Results found that METTL3 wasup-regulated in the breast cancer tissue and cells. In vivo and vitro, METTL3knockdown could decrease the methylation level, reduce the proliferation, acceleratethe apoptosis and inhibited the tumor growth. Moreover, we found that Bcl-2 acted asthe target of METTL3, thereby regulating the proliferation and apoptosis of breastcancer. This study could reveal the potential mechanism of m6A modification in thebreast cancer tumorigenesis, providing potential drug targets in the treatment.CI - Copyright © 2019 Elsevier B.V. All rights reserved.



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