Long non-coding RNA (lncRNA) TTN antisense RNA 1 (TTN-AS1) was reported to be crucial modulators in the tumorigenesis of several types of cancers. However, it is unclear whether TTN-AS1 can regulate the progression of ovarian cancer (OC). The present study aimed to explore functional roles and molecular mechanism of TTN-AS1 in OC. Quantitative reverse transcriptase-polymerase chain reaction assay (qRT-PCR) was used to detect the expression of TTN-AS1 in OC tissues and cell lines. The biological function of TTN-AS1 in OC was identified by a series of in vitro and in vivo assays. Bioinformatics analysis and mechanism experiments were used to analyze and identify the molecular mechanism of TTN-AS1 in OC progression. A high level of TTN-AS1 was found in OC tissues and cell lines. High TTN-AS1 was positively associated with advanced FIGO stage, lymph node metastasis, and poorer overall survival of OC patients. Functionally, knockdown of TTN-AS1 inhibited cell proliferation, colony formation, invasion and migration of OC cells in vitro, and suppressed tumor formation in vivo. Mechanistically, TTN-AS1 functioned as a competing endogenous RNA by sponging microRNA-139-5p (miR-139-5p) to elevate Rho-associated coiled-coil containing protein kinase 2 (ROCK2). Downregulation of miR-139-5p or upregulation of ROCK2 partially rescued the inhibitory impact of TTN-AS1 knockdown on OC cells. These results obtained in the present study suggested that TTN-AS1 promoted the progression of OC by regulating the miR-139-5p/ROCK2 axis.
Copyright © 2020 The Authors. Published by Elsevier Masson SAS.. All rights reserved.