生物
基因敲除
癌变
乳腺癌
甲基转移酶
癌症研究
细胞凋亡
机制(生物学)
癌症
甲基化
体内
细胞生物学
生物化学
遗传学
基因
哲学
认识论
作者
Hong Wang,Bei Xu,Jun Shi
出处
期刊:Gene
[Elsevier]
日期:2020-01-01
卷期号:722: 144076-144076
被引量:165
标识
DOI:10.1016/j.gene.2019.144076
摘要
N6-methyladenosine (m6A) is the most prevalent internal modification in mammalian mRNAs and methyltransferase-like 3 (METTL3) is a vital methyltransferase in m6A modification. Here, this study tries to discover the regulatory role of METTL3 and its mechanism in the breast cancer tumorigenesis. Results found that METTL3 was up-regulated in the breast cancer tissue and cells. In vivo and vitro, METTL3 knockdown could decrease the methylation level, reduce the proliferation, accelerate the apoptosis and inhibited the tumor growth. Moreover, we found that Bcl-2 acted as the target of METTL3, thereby regulating the proliferation and apoptosis of breast cancer. This study could reveal the potential mechanism of m6A modification in the breast cancer tumorigenesis, providing potential drug targets in the treatment.
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