N6-methyladenine- induced LINC00667 promoted breast cancer progression through m6A/KIAA1429 positive feedback loop. Issue 5 (2nd May 2022)

• Record Type: Journal Article
• Authors: Ren, Saiyu; Zhang, Yuxing; Yang, Xiaodong; Li, Xue; Zheng, Yuexin; Liu, Yun; Zhang, Xiliang
• Is Part Of: Bioengineered. Volume 13:Issue 5(2022)
• Page Start: 13462
• Page End: 13473
• Publication Date: 2022-05-02
• Subjects: N6-methyladenosine -- breast cancer -- LINC00667 -- METTL3; Biomedical engineering -- Periodicals; Biotechnology -- Periodicals; Microbiology -- Periodicals; 660.6
• DOI: 10.1080/21655979.2022.2077893
• Languages: English
• ISSNs: 2165-5987

Abstract

ABSTRACT: Increasing evidence supports that N 6 -methyladenine (m 6 A) and long noncoding RNAs (lncRNAs) both act as master regulators involved in breast cancer (BC) tumorigenesis at epigenetic modification level. Here, our research tries to unveil the interaction of m 6 A and lncRNAs on BC progression and explore the underlying regulatory mechanism. In the current study, we found that LINC00667 was m 6 A-modified lncRNA, which was up-regulated upon the overexpression of KIAA1429. The high expression of LINC00667 was correlated with the prognosis of BC patients. Bio-functional assays indicated that LINC00667 promoted the proliferation and migration of BC cells. Mechanistic assays illustrated that KIAA1429 targeted the m 6 A modification site of LINC00667 and enhanced its mRNA stability. Moreover, LINC00667 positively regulated the KIAA1429 via sponging miR-556-5p, forming a KIAA1429/m 6 A/LINC00667/miR-556-5p feedback loop. Collectively, the central findings of our study suggest that KIAA1429-induced LINC00667 exerted its functions as an oncogene in BC progression through m 6 A-dependent feedback loop. Graphical abstract: uf0001