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Long noncoding RNA (lncRNA) is emerging as an essential regulator in the development and progression of cancer, including cervical cancer (CC). In this study, we found a CC-related lncRNA, KCNMB2-AS1, which was significantly overexpressed in CC and linked to poor outcomes. Depletion of KCNMB2-AS1 remarkably inhibited CC cell proliferation and induced apoptosis. In vivo xenograft models revealed that knockdown of KCNMB2-AS1 evidently delayed tumor growth. Mechanistically, KCNMB2-AS1 was predominantly located in the cytoplasm and served as a competing endogenous RNA to abundantly sponge miR-130b-5p and miR-4294, resulting in the upregulation of IGF2BP3, a well-documented oncogene in CC. Moreover, IGF2BP3 was able to bind KCNMB2-AS1 by three N 6 -methyladenosine (m 6 A) modification sites on KCNMB2-AS1, in which IGF2BP3 acted as an m 6 A “reader” and stabilized KCNMB2-AS1. Thus, KCNMB2-AS1 and IGF2BP3 formed a positive regulatory circuit that enlarged the tumorigenic effect of KCNMB2-AS1 in CC. Together, our data clearly suggest that KCNMB2-AS1 is a novel oncogenic m 6 A-modified lncRNA in CC, targeting KCNMB2-AS1 and its related molecules implicate the therapeutic possibility for CC patients.

cell transplantation

Long Noncoding RNA KCNMB2-AS1 Stabilized by N<sup>6</sup>-Methyladenosine Modification Promotes Cervical Cancer Growth Through Acting as a Competing Endogenous RNA

Long Noncoding RNA KCNMB2-AS1 Stabilized by N6-Methyladenosine Modification Promotes Cervical Cancer Growth Through Acting as a Competing Endogenous RNA

Long Noncoding RNA KCNMB2-AS1 Stabilized by N⁶-Methyladenosine Modification Promotes Cervical Cancer Growth Through Acting as a Competing Endogenous RNA