m6A-induced LINC00958 promotes breast cancer tumorigenesis via the miR-378a-3p/YY1 axis

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作者
Dongwen Rong
Qian Dong
Huajun Qu
Xinna Deng
Fei Gao
Qingxia Li
Ping Sun
机构
[1] the First Hospital of Shanxi Medical University,Department of Oncology
[2] The Fourth Hospital of Hebei Medical University,Department of Internal Oncology
[3] Yantai Yuhuangding Hospital,Department of Oncology
[4] The Fourth Department of Oncology,undefined
[5] Hebei General Hospital,undefined
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Increasing evidence demonstrates that long noncoding RNAs (lncRNAs) play critical roles in human breast cancer (BC) tumorigenesis. However, the mechanisms by which lncRNA and N6-methyladenosine (m6A) regulate BC tumorigenesis are still unclear. In the present research, LINC00958 was markedly overexpressed in BC tissue and cells, and LINC00958 upregulation promoted the tumor progression of BC cells. Mechanistically, m6A methyltransferase-like 3 (METTL3) gave rise to the upregulation of LINC00958 by promoting its RNA transcript stability. Moreover, LINC00958 acted as a competitive endogenous RNA for miR-378a-3p to promote YY1. Overall, these data provide novel insight into how m6A-mediated LINC00958 regulates BC tumorigenesis.
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