基因敲除
下调和上调
组织蛋白酶L
转移
癌症研究
信使核糖核酸
甲基转移酶
宫颈癌
癌症
生物
细胞生物学
化学
医学
组织蛋白酶
内科学
细胞凋亡
基因
酶
生物化学
甲基化
作者
Pingping Liu,Mingxiu Ju,Xiaojing Zheng,Yinan Jiang,Xing-Juan Yu,Baoyue Pan,Rongzhen Luo,Wei‐Hua Jia,Min Zheng
出处
期刊:Cancer Science
[Wiley]
日期:2022-11-16
卷期号:114 (3): 837-854
被引量:11
摘要
N6-methyladenosine (m6A) is a highly abundant RNA modification in eukaryotic cells. Methyltransferase-like 3 (METTL3), a major protein in the m6A methyltransferase complex, plays important roles in many malignancies, but its role in cervical cancer metastasis remains uncertain. Here, we found that METTL3 was significantly upregulated in cervical cancer tissue, and its upregulation was associated with a poor prognosis in cervical cancer patients. Knockdown of METTL3 significantly reduced cervical cancer cell migration and invasion. Conversely, METTL3 overexpression markedly promoted cervical cancer cell metastasis in vitro and in vivo. Furthermore, METTL3 mediated the m6A modification of cathepsin L (CTSL) mRNA at the 5'-UTR, and the m6A reader protein insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) bound to the m6A sites and enhanced CTSL mRNA stability. Our results indicated that METTL3 enhanced CTSL mRNA stability through an m6A-IGF2BP2-dependent mechanism, thereby promoting cervical cancer cell metastasis. These findings provide insights into a novel m6A modification pattern involved in cervical cancer development.
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