BACKGROUND Circular RNAs (circRNAs) are pivotal in cancer biology. Nevertheless, the biological functions of circular RNA hsa_circ_0000437 (circ_0000437) have not yet been elucidated. INTRODUCTION In the present study, we studied… Click to show full abstract
BACKGROUND Circular RNAs (circRNAs) are pivotal in cancer biology. Nevertheless, the biological functions of circular RNA hsa_circ_0000437 (circ_0000437) have not yet been elucidated. INTRODUCTION In the present study, we studied the expression characteristics of circ_0000437 in endometrial carcinoma (EC) and explored the roles and potential mechanisms of circ_0000437 in EC progression. METHODS Quantitative real-time polymerase chain reaction (qRT-PCR) was adopted to detect the expressions of circ_0000437, microRNA-626 (miR-626) and cyclin-dependent kinase inhibitor 1B (CDKN1B) in EC tissues and cells. 5-Ethynyl-2'-deoxyuridine (EdU), cell counting kit-8 (CCK-8) and Transwell assays were performed to evaluate EC cell proliferation and invasion. The expressions of CDKN1B and epithelial-mesenchymal transition (EMT)-related proteins (E-cadherin and N-cadherin) were detected by Western blot. Moreover, the targeted relationship between miR-626 and circ_0000437 or CDKN1B was determined by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. RESULTS Circ_0000437 expression was reduced in EC tissues, and the low expression of circ_0000437 was positively correlated with the lymph node metastasis and high TNM stage of EC patients. Knocking down circ_0000437 promoted the proliferation, invasion and EMT of EC cells. Circ_0000437 directly targeted miR-626 and negatively modulated miR-626 expression in EC cells. CDKN1B was identified as the downstream target of miR-626 in EC cells. Besides, CDKN1B overexpression or miR-626 knockdown reversed the effects of knocking down circ_0000437 on EC cells. CONCLUSION Circ_0000437 regulates the miR-626/CDKN1B pathway to suppress the proliferation, invasion and EMT of EC cells. This indicates that circ_0000437 may be a promising biomarker and therapy target for EC.
               
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