Abstract
Long non-coding RNAs (lncRNAs) are identified as vital modulators in a number of biological processes, including tumorigenesis. However, the role of lncRNAs in endometrial carcinoma (EC) remains unknown. In the current study, the expression patterns, biological roles and functional mechanism of the lncRNA colon cancer associated transcript 1 (CCAT1) was examined in EC. The expression level of CCAT1 was significantly upregulated in EC tissue samples compared with matched adjacent healthy tissue samples from patients with endometrial cancer. Similarly, CCAT1 was significantly upregulated in several EC cell lines (KLE, Ishiwaka and HEC-1-A), compared with the normal human endometrial stromal cell line T-HESC. Cell counting kit-8 and Transwell migration assays demonstrated that CCAT1 knockdown significantly decreased EC cell proliferation and migration. In addition, CCAT1 was confirmed as a target gene of miR-181a-5p in EC. Overexpression of miR-181a-5p significantly decreased CCAT1 expression in EC cells, whilst knockdown of CCAT1 significantly increased miR-181a-5p expression in EC cells. Furthermore, miR-181a-5p expression was significantly downregulated in EC tissue samples compared with matched adjacent healthy tissue samples from patients with endometrial cancer. Similarly, miR-181a-5p expression was significantly downregulated in several EC cell lines (KLE, Ishiwaka and HEC-1-A), compared with normal human endometrial stromal cell line T-HESC. In addition, rescue experiments demonstrated that inhibition of miR-181a-5p significantly reversed the effect of CCAT1 knockdown on EC cell proliferation and migration. The results suggest that CCAT1 promotes EC progression by acting as a molecular sponge of miR-181a-5p.