Promotive actions of lncRNA EBLN3P involved in cervical cancer progression via interacting with miR-29c-3p and TAF15 to modify RCC2

Abstract

BackgroundCervical cancer is a common cancer that seriously affects women's health globally. The key roles of long non-coding RNAs (lncRNAs) in the onset and development of cervical cancer have attracted much attention. Our study aims to uncover the roles of lncRNA EBLN3P and miR-29c-3p and the mechanisms by which EBLN3P and miR-29c-3p regulate malignancy in cervical cancer. MethodsTumor and adjacent normal tissues were collected from cervical cancer patients, and the expression of EBLN3P and miR-29c-3p were analyzed via RT-qPCR. The capacities of proliferation, migration, and invasion were assessed using CCK-8, wound healing and transwell assays. The interaction among EBLN3P, miR-29c-3p and TAF15 was determined by luciferase, RNA immunoprecipitation and RNA pull-down assays, respectively. A subcutaneous tumor xenograft mouse model was established to evaluate the functional role of EBLN3P in vivo. ResultsThe interaction and reciprocal negative regulation between EBLN3P and miR-29c-3p were uncovered in cervical cancer cells. Likewise, EBLN3P and miR-29c-3p expression patterns in tumor tissues presented a negative association. EBLN3P knockdown weakened cell proliferation, migration and invasion, but these effects were abrogated by miR-29c-3p depletion. Mechanistically, ALKBH5 might impaired EBLN3P stability to reduce its expression. EBLN3P functioned as a competing endogenous RNA (ceRNA) for miR-29c-3p to relieve its suppression of RCC2. Besides, EBLN3P enhanced RCC2 mRNA stability via interacting with TAF15. Furthermore, silencing of EBLN3P repressed the tumor growth in mice. ConclusionAltogether, lncRNA EBLN3P positively regulates RCC2 expression via competitively binding to miR-29c-3p and interacting with TAF15, thereby boosting proliferation, migration, and invasion of cervical cancer cells.