Circ_0004712 promotes endometriotic epithelial cell proliferation,migration and invasion by regulating miR-488-3p/ROCK1 axis in vitro |
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| Institution: | 1. Department of Reproductive Center, Changzhou Maternal and Child Health Care Hospital, Changzhou Medical Center, Nanjing Medical University, Changzhou City, Jiangsu Province, China;2. Department of Gynecology, Changzhou Maternal and Child Health Care Hospital, Changzhou Medical Center, Nanjing Medical University, Changzhou City, Jiangsu Province, China;1. Laboratorio de Medicina Reproductiva, Universidad Nacional de Rosario, Suipacha 531, C.P: 2000, Rosario, Santa Fe, Argentina;2. Consejo de Investigaciones de la Universidad Nacional de Rosario (CIUNR), Rosario, Santa Fe, Argentina;3. Consejo Nacional de Investigaciones Científicas y Técnicas, CONICET, Rosario, Santa Fe, Argentina;1. Department of Biochemistry and Molecular Biology, Medical School, Southeast University, #87 Dingjiaqiao Road, Gulouqu, Nanjing, Jiangsu Province 210009, China;2. Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, Guangxi 533000, China;3. Environmental Health Risk Assessment and Prevention Engineering Center of Ecological Aluminum Industry Base of Youjiang Medical University for Nationalities, Baise, Guangxi 533000, China;4. Pharmacology Department, Xinjiang Medical University, #393, Xinyi Road, Xinshiqu, Urumqi, Xinjiang 830011, China;1. Department of Obstetrics and Gynecology, Clinical Medical College, Yangzhou University, Yangzhou 225001, China;2. State Key Laboratory of Reproductive Medicine, Clinical Center of Reproductive Medicine, First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, China;1. Laboratory of Genetics and Evolution, Institute of Zoology and Biomedical Research, Jagiellonian University, Krakow, Poland;2. Forensic Genetics Section, Institute of Forensic Research, Krakow, Poland;3. Deptartment of Molecular Neuropharmacology, Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland;4. Max-Delbrück-Center for Molecular Medicine (MDC) in the Helmholtz Association, Berlin, Germany;5. Department of Molecular Biology, Institute of Genetics and Animal Biotechnology, Polish Academy of Sciences Jastrz?biec, Magdalenka, Poland;1. Isotope Research Lab, Biological Engineering and Application Biology Department, Sichuan Agricultural University, Ya’an 625014, China;2. Key Laboratory for Animal Disease-Resistant Nutrition of the Ministry of Education of China, Animal Nutrition Institute, Sichuan Agricultural University, Chengdu 611130, China |
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| Abstract: | Recent evidence indicates that circular RNAs (circRNAs) play crucial regulatory roles in the pathogenesis and development of endometriosis. Circ_0004712 was found to be differentially expressed in endometriosis. However, the detailed function and mechanism of circ_0004712 in endometriosis are still unclear. Quantitative real-time polymerase chain reaction and Western blot were used for the detection of circ_0004712, miR-488-3p and ROCK1 (Rho Associated Coiled-Coil Containing Protein Kinase 1) levels. In vitro experiments in endometrial endothelial cells were performed by cell counting kit-8, EdU, transwell, wound healing assays, and flow cytometry, respectively. The molecular mechanism of circ_0004712 function was investigated using bioinformatics target predication, dual-luciferase reporter, and RNA immunoprecipitation (RIP) assays. The expression of circ_0004712 was higher in endometriotic endometrial tissues and epithelial cells. Knockdown of circ_0004712 suppressed cell proliferation, migration, invasion, EMT process and induced apoptosis in ectopic endometrial epithelial cells in vitro. Mechanistically, circ_0004712 acted as a ceRNA to sponge miR-488-3p, thus elevating the expression of ROCK1, which was confirmed to be a target of miR-488-3p. Rescue experiments suggested that miR-488-3p inhibition reversed the inhibitory effects of circ_0004712 silencing on cell growth and metastasis. Moreover, miR-488-3p restoration restrained the proliferation and metastasis in ectopic endometrial epithelial cells, which were attenuated by ROCK1 overexpression. Circ_0004712 knockdown suppressed the proliferation and metastasis of ectopic endometrial epithelial cells via miR-488-3p/ROCK1 axis in vitro, suggesting a new insight into the pathogenesis of endometriosis. |
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| Keywords: | Circ_0004712 MiR-488-3p ROCK1 Endometriosis Epithelial cells |
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