Abstract
Endometrial cancer (EC) is one of the most common gynecological tumors with an increasing incidence. CircRNA plays an essential regulatory role in EC. Our objective was to investigate the potential mechanism of circRNAs derived SPOC Domain Containing 1 (SPOCD1) in EC progression. Seven circRNAs from SPOCD1 were analyzed by circBase and their expression was verified by quantitative real-time polymerase chain reaction. Only the expression of hsa_circ_0011324 was significantly increased in cancer tissues. The cell lines Ishikawa and RL95-2 which interfered with or overexpressed hsa_circ_0011324 were constructed and cell functions were tested. Results revealed hsa_circ_0011324 overexpression promoted cell proliferation, migration, and invasion; while silence of hsa_circ_0011324 had opposite effect on cell functions. RNA22 website and Targetscan website were applied to analyze downstream genes regulated by hsa_circ_0011324. Then, the expression of downstream genes was detected in EC tissues. Results indicated hsa-miR-497/16-5p expression were down-regulated, and mechanistic target of rapamycin kinase (mTOR) was up-regulated in EC. Furthermore, hsa_circ_0011324 regulated mTOR expression and cell functions by affecting hsa-miR-497/16-5p. And the potential mechanism was hsa_circ_0011324 competes with mTOR to directly bind to hsa-miR-497/16-5p. In conclusion, hsa_circ_0011324 could sponge hsa-miR-497/16-5p targeted mTOR to participate in EC progress. Our study may provide a new therapeutic target for EC.