Zhizhen Wang1,2,3, Yang Chen1,2,3, Wei Wang1,2,3, Hui Wang4, Ransheng Liu1,2,3. 1. Department of Radiation Oncology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer Tianjin, China. 2. Key Laboratory of Cancer Prevention and Therapy Tianjin, China. 3. Tianjin's Clinical Research Center for Cancer Tianjin, China. 4. Department of Radiology, Tianjin Third Central Hospital Tianjin, China.
Abstract
OBJECTIVE: To analyze the role of circMYC in cervical cancer. METHODS: Protein and RNA expression was detected by RT-qPCR and western blotting. Transwell, CCK8, and colony formation assays were used for measuring metastasis, cell viability, and proliferation, respectively. Lactate production, glucose uptake, and ATP generation were examined to evaluate cell glycolysis. Interactions between circMYC, miR-577, and MET were determined by RNA pull-down and immunoprecipitation, and dual-luciferase reporter assays. Xenografts were established in mice to evaluate the functions of circMYC in vivo. RESULTS: circMYC was overexpressed in tumor tissue, which was related to poor prognosis. CircMYC knockdown reduced proliferation, colony formation, metastasis, and glycolysis in cervical cancer cells as well as inhibiting tumor growth in vivo. Mechanistically, circMYC targeted miR-577, and the effects of circMYC knockdown could be reversed by miR-577 inhibition. Moreover, miR-577 downregulated the expression of MET. Therefore, the oncogenic role of circMYC in cervical cancer was achieved by sponging miR-577 and maintaining MET expression. CONCLUSION: circMYC promotes cervical cancer progression through regulation of the miR-577/MET axis. circMYC may thus be a potential target for diagnosing and treating cervical cancer. AJTR
OBJECTIVE: To analyze the role of circMYC in cervical cancer. METHODS: Protein and RNA expression was detected by RT-qPCR and western blotting. Transwell, CCK8, and colony formation assays were used for measuring metastasis, cell viability, and proliferation, respectively. Lactate production, glucose uptake, and ATP generation were examined to evaluate cell glycolysis. Interactions between circMYC, miR-577, and MET were determined by RNA pull-down and immunoprecipitation, and dual-luciferase reporter assays. Xenografts were established in mice to evaluate the functions of circMYC in vivo. RESULTS: circMYC was overexpressed in tumor tissue, which was related to poor prognosis. CircMYC knockdown reduced proliferation, colony formation, metastasis, and glycolysis in cervical cancer cells as well as inhibiting tumor growth in vivo. Mechanistically, circMYC targeted miR-577, and the effects of circMYC knockdown could be reversed by miR-577 inhibition. Moreover, miR-577 downregulated the expression of MET. Therefore, the oncogenic role of circMYC in cervical cancer was achieved by sponging miR-577 and maintaining MET expression. CONCLUSION: circMYC promotes cervical cancer progression through regulation of the miR-577/MET axis. circMYC may thus be a potential target for diagnosing and treating cervical cancer. AJTR
Authors: Teng Li; Yi Xing; Fan Yang; Yangyang Sun; Shaojin Zhang; Qingwei Wang; Weixing Zhang Journal: Cancer Med Date: 2020-04-05 Impact factor: 4.452