Long non-coding RNA RP11-552M11.4 favors tumorigenesis and development of cervical cancer via modulating miR-3941/ATF1 signaling.

Abstract

As one of the most aggressive malignancies, cervical cancer (CC) which mainly affects females has high risks of relapse and death. Long non-coding RNA (lncRNA) RP11-552M11.4 is verified to promote the progression of ovarian cancer; nevertheless, its role and the probable molecular mechanisms in CC remain unclear until the present study. Herein, we unveiled that the expression of lncRNA RP11-552M11.4 tested by qRT-PCR was enhanced in tumor tissues compared with the para-carcinoma tissues and related to FIGO Stage, lymph node metastasis, vascular invasion and distant metastasis in CC. Additionally, CC patients with high lncRNA RP11-552M11.4 level suffered from poor clinical outcomes. Moreover, silenced lncRNA RP11-552M11.4 restrained cell proliferation, migration and invasion in CC cells. Subsequently, the mechanistic studies revealed that lncRNA RP11-552M11.4 functioned as a ceRNA of ATF1 in CC by acting as the endogenous sponge for miR-3941, which was identified as a tumor suppressor in CC. Moreover, both miR-3941 inhibition and ATF1 overexpression restored the impacts of inhibited lncRNA RP11-552M11.4 on cellular processes in CC cells. Our observations elucidated the carcinogenic role of lncRNA RP11-552M11.4 in CC was mediated through miR-3941/ATF1 axis, giving a new insight into the effective target for the treatment and prognosis of cervical cancer.