LINC00702 accelerates the progression of ovarian cancer through interacting with EZH2 to inhibit the transcription of KLF2.

Abstract

To clarify the role of LINC00702 in the progression of ovarian cancer (OC) and the potential mechanism. Expression level of LINC00702 in OC tissues and matched normal tissues was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). LINC00702 level in OC cell lines was determined as well. The potential influences of LINC00702 on cellular behaviors of A2780 and HEY cells were evaluated. The subcellular distribution of LINC00702 in A2780 cells was examined. Through RNA immunoprecipitation (RIP) and Chromatin immunoprecipitation (ChIP) assay, the interaction among LINC00702, EZH2, and KLF2 was verified. The rescue experiments were conducted to elucidate the biological function of LINC00702/KLF2 axis in the progression of OC. LINC00702 was upregulated in OC tissues and cell lines. Its level was much higher in OC with worse tumor stage and larger tumor size. The knockdown of LINC00702 attenuated the proliferative ability of A2780 and HEY cells. LINC00702 was mainly distributed in the cell nucleus. The knockdown of LINC00702 or EZH2 downregulated the KLF2 level in the OC cells. The transfection of LINC00702 markedly reduced the occupancy of KLF2 promoter on EZH2 and H3K27me3 relative to IgG. Finally, the knockdown of KLF2 could reverse the regulatory effect of LINC00702 in the proliferative ability of A2780 cells. LINC00702 is upregulated in OC. It accelerates the progression of OC via interacting with EZH2 to inhibit the transcription of KLF2.