N6-methyladenosine METTL3 promotes the breast cancer progression via targeting Bcl-2
N6-methyladenosine METTL3 promotes the breast cancer progression via targeting Bcl-2
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DOI：
10.1016/j.gene.2019.144076
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发表时间：
2020-01-05
期刊：
影响因子：
3.5
通讯作者：
Shi, Jun
中科院分区：
文献类型：
--
作者：
Wang, Hong;Xu, Bei;Shi, Jun
n6 -甲基腺苷（m6A）是哺乳动物mrna中最常见的内部修饰，甲基转移酶样3 （METTL3）是m6A修饰中重要的甲基转移酶。本研究试图发现METTL3在乳腺癌肿瘤发生中的调控作用及其机制。结果发现METTL3在乳腺癌组织和细胞中表达上调。在体内和体外实验中，敲低METTL3可降低甲基化水平，抑制肿瘤增殖，加速细胞凋亡，抑制肿瘤生长。此外，我们发现Bcl-2作为METTL3的靶点，从而调节乳腺癌的增殖和凋亡。本研究可揭示m6A修饰在乳腺癌肿瘤发生中的潜在机制，为乳腺癌治疗提供潜在的药物靶点。
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.