W Tong1, T-C Han, W Wang, J Zhao. 1. Department of Thoracic Surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, China. tianci2010@vip.qq.com.
Abstract
OBJECTIVE: To elucidate whether long non-coding RNA cancer susceptibility candidate 11 (lncRNA CASC11) could participate in the development of lung cancer through targeting microRNA-302/CDK1 axis. PATIENTS AND METHODS: Expression levels of CASC11, microRNA-302 and CDK1 in lung cancer tissues and paracancerous tissues were determined by quantitative real-time polymerase chain reaction (qRT-PCR). CASC11 expression in lung cancer cell lines was also determined. The regulatory effect of CASC11 on proliferative potential of lung cancer cells was accessed by cell counting kit-8 (CCK-8) and colony formation assay. The binding condition between microRNA-302 to CASC11 and CDK1 was evaluated by dual-luciferase reporter gene assay. CDK1 expression in lung cancer cells with CASC11 or microRNA-302 knockdown was detected by Western blot. The proliferation of lung cancer cells was determined after transfection of microRNA-302 inhibitor or co-transfection of microRNA-302 inhibitor and si-CASC11. RESULTS: CASC11 and CDK1 were highly expressed, whereas microRNA-302 was lowly expressed in lung cancer tissues. Identically, CASC11 was highly expressed in lung cancer cell lines (A547, H157 and SPC-A-1) than controls as well. CASC11 knockdown attenuated proliferative capacity of lung cancer cells. The opposite trend was observed by microRNA-302 knockdown. Dual-luciferase reporter gene assay verified that CASC11 could bind to microRNA-302 and microRNA-302 could bind to CDK1. CDK1 expression in lung cancer cells was negatively regulated by CASC11. MicroRNA-302 knockdown reversed the inhibitory effect of CASC11 on CDK1 expression. The proliferation of lung cancer cells co-transfected with microRNA-302 inhibitor and si-CASC11 decreased compared with those transfected with microRNA-302 inhibitor. CONCLUSIONS: High expression of CASC11 promotes the development of lung cancer through upregulating CDK1 expression by binding to microRNA-302.
OBJECTIVE: To elucidate whether long non-coding RNA cancer susceptibility candidate 11 (lncRNA CASC11) could participate in the development of lung cancer through targeting microRNA-302/CDK1 axis. PATIENTS AND METHODS: Expression levels of CASC11, microRNA-302 and CDK1 in lung cancer tissues and paracancerous tissues were determined by quantitative real-time polymerase chain reaction (qRT-PCR). CASC11 expression in lung cancer cell lines was also determined. The regulatory effect of CASC11 on proliferative potential of lung cancer cells was accessed by cell counting kit-8 (CCK-8) and colony formation assay. The binding condition between microRNA-302 to CASC11 and CDK1 was evaluated by dual-luciferase reporter gene assay. CDK1 expression in lung cancer cells with CASC11 or microRNA-302 knockdown was detected by Western blot. The proliferation of lung cancer cells was determined after transfection of microRNA-302 inhibitor or co-transfection of microRNA-302 inhibitor and si-CASC11. RESULTS:CASC11 and CDK1 were highly expressed, whereas microRNA-302 was lowly expressed in lung cancer tissues. Identically, CASC11 was highly expressed in lung cancer cell lines (A547, H157 and SPC-A-1) than controls as well. CASC11 knockdown attenuated proliferative capacity of lung cancer cells. The opposite trend was observed by microRNA-302 knockdown. Dual-luciferase reporter gene assay verified that CASC11 could bind to microRNA-302 and microRNA-302 could bind to CDK1. CDK1 expression in lung cancer cells was negatively regulated by CASC11. MicroRNA-302 knockdown reversed the inhibitory effect of CASC11 on CDK1 expression. The proliferation of lung cancer cells co-transfected with microRNA-302 inhibitor and si-CASC11 decreased compared with those transfected with microRNA-302 inhibitor. CONCLUSIONS: High expression of CASC11 promotes the development of lung cancer through upregulating CDK1 expression by binding to microRNA-302.