三阴性乳腺癌
基因敲除
Wnt信号通路
癌症研究
乳腺癌
连环素
癌变
生物
癌症
细胞生长
细胞凋亡
信号转导
医学
内科学
细胞生物学
遗传学
作者
Xiang Yu,Yaxun Li,Fanshuang Kong,Qing‐Long Xu
标识
DOI:10.1016/j.tiv.2023.105746
摘要
N6-methyladenosine (m6A) modification, the most abundant methylation modification on eukaryotic mRNAs, was implicated in the tumourigenesis. This study aimed to explore the role of methyltransferase like 3 (METTL3) in triple-negative breast cancer progression and its underlying mechanisms. FAM83D was markedly elevated in triple-negative breast cancer tissues and cells, and high expression of FAM83D was related to the poor prognosis of triple-negative breast cancer patients. FAM83D knockdown significantly retarded cell proliferation, invasion, stemness, and accelerated cell apoptosis in triple-negative breast cancer cells. On the contrary, overexpression of FAM83D promoted the malignant behaviors. METTL3 could interact with FAM83D and mediate m6A modification of FAM838D. Moreover, METTL3 positively regulated FAM83D expression, and FAM83D overexpression could block the inhibition effects of MRTTL3 knockdown on the malignant behaviors. METTL3 knockdown decreased FAM83D expression to inhibit the Wnt/β-catenin pathway. In addition, knockdown of FAM83D also showed the repressive effects on tumor growth in triple-negative breast cancer in vivo. These findings suggested that METTL3 could modulate FAM83D protein expression through m6A modification to aggravate triple-negative breast cancer progression via the Wnt/β-catenin pathway.
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