J-J Dai C Tian1, L Liang. 1. Department of Gynecology, the First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui, China. daijunjun_doctor@tom.com.
Abstract
OBJECTIVE: Circular RNAs (circRNAs) have emerged as crucial regulators for tumor progression. However, the effects of circRNAs are not entirely clear in cervical cancer (CC). The objective of this study was to investigate the function and regulation mechanism of circular RNA SMARCA5 (circSMARCA5, also named hsa_circ_0001445) in cervical cancer. PATIENTS AND METHODS: circSMARCA5 and miR-620 expressions were analyzed by qRT-PCR assay. The cell proliferation, cell cycle, migration, invasion abilities were measured by CCK-8 and colony formation, Flow cytometry, Wound-healing and transwell assays. In addition, the interaction between circSMARCA5 and miR-620 was accessed by luciferase reporter assay. RESULTS: The results indicated that circSMARCA5 was downregulated in CC; overexpression of circSMARCA5 inhibited CC cell proliferation, migration and invasion, and induced cell cycle arrest. In addition, we found that circSMARCA5 could bind to miR-620 and significantly downregulated its expression. Furthermore, the results revealed that circSMARCA5 suppressed proliferation and invasion by miR-620 in CC. CONCLUSIONS: We suggested that circSMARCA5/miR-620 regulatory axis is involved in the development of CC and may serve as a potential therapy target.
OBJECTIVE: Circular RNAs (circRNAs) have emerged as crucial regulators for tumor progression. However, the effects of circRNAs are not entirely clear in cervical cancer (CC). The objective of this study was to investigate the function and regulation mechanism of circular RNA SMARCA5 (circSMARCA5, also named hsa_circ_0001445) in cervical cancer. PATIENTS AND METHODS: circSMARCA5 and miR-620 expressions were analyzed by qRT-PCR assay. The cell proliferation, cell cycle, migration, invasion abilities were measured by CCK-8 and colony formation, Flow cytometry, Wound-healing and transwell assays. In addition, the interaction between circSMARCA5 and miR-620 was accessed by luciferase reporter assay. RESULTS: The results indicated that circSMARCA5 was downregulated in CC; overexpression of circSMARCA5 inhibited CC cell proliferation, migration and invasion, and induced cell cycle arrest. In addition, we found that circSMARCA5 could bind to miR-620 and significantly downregulated its expression. Furthermore, the results revealed that circSMARCA5 suppressed proliferation and invasion by miR-620 in CC. CONCLUSIONS: We suggested that circSMARCA5/miR-620 regulatory axis is involved in the development of CC and may serve as a potential therapy target.