LncRNA KCNQ1OT1‐mediated cervical cancer progression by sponging miR‐1270 as a ceRNA of LOXL2 through PI3k/Akt pathway

摘要

Abstract Background Dysregulated noncoding RNAs participated in progressions of cervical cancer. Purpose To verify impacts of KCNQ1OT1 on modulating progressions of cervical cancer cells. Method Expressions of KCNQ1OT1, miR‐1270, and LOXL2 were analyzed through RT‐qPCR and protein expressions of LOXL2, p‐AKT, and AKT were validated using western blot. Bindings of miR‐1270 with KCNQ1OT1 or LOXL2 were verified using luciferase reporter assay. CCK‐8 and flow cytometry evaluated cell viability and apoptosis, respectively. The PI3K/AKT signaling pathway suppressor, LY294002, was applied to treat the cells and the changes of KCNQ1OT1 expression and LOXL2, p‐AKT, and AKT protein expressions were examined. Results KCNQ1OT1 expression was the highest in HeLa cells but lowest in SiHa cells whose upregulation improved the viability but inhibited the apoptosis in SiHa cells while knockdown of KCNQ1OT1 caused opposite results in HeLa cells. MiR‐1270 was sponged and negatively modulated by KCNQ1OT1. MiR‐1270 mimics caused low viability and high apoptosis of SiHa cells but miR‐1270 inhibitor reverse its roles in HeLa cells. LOXL2, the target of miR‐1270, positively interplayed with KCNQ1OT1 but had negative interaction with miR‐1270. LOXL2 overexpression promoted viability and decreased apoptosis of SiHa cells but knockdown of LOXL2 restored its effects in HeLa cells. Moreover, LOXL2 and phosphorylated AKT (p‐AKT) protein expressions were downregulated by suppressed KCNQ1OT1 and LOXL2 and miR‐1270 mimics but promoted by overexpressed KCNQ1OT1 and LOXL2 and miR‐1270 inhibitor. Additionally, LY294002 treatment caused low KCNQ1OT1 RNA expression and decreased LOXL2 and p‐AKT protein expressions. Conclusion KCNQ1OT1/miR‐1270/LOXL2 axis modulated viability and apoptosis of cervical cancer cells.