RESUMO
BACKGROUND: Cervical cancer (CC) is a common gynecological tumor that affects women's health. Circular RNA hsa_circ_0084927 (hsa_circ_0084927) has been reported to be upregulated in CC. However, the role and regulatory mechanism of hsa_circ_0084927 in CC are unclear. METHODS: Expression of hsa_circ_0084927, microRNA (miR)-634, and tumor protein D52 (TPD52) mRNA in CC tissues and cells was examined by quantitative real-time polymerase chain reaction (qRT-PCR). The proliferation, colony formation, cell cycle progression, apoptosis, migration, and invasion of CC cells were determined with cell counting kit-8 (CCK-8), plate clone, flow cytometry, or transwell assays. The levels of cyclin D1, cleaved-caspase-3 (c-caspase 3), matrix metalloproteinase (MMP)-2, MMP-9, and TPD52 protein were evaluated with Western blotting. The targeting relationship between hsa_circ_0084927 or TPD52 and miR-634 was verified via dual-luciferase reporter and/or RNA immunoprecipitation (RIP) assays. Xenograft assay was conducted to confirm the role of hsa_circ_0084927 in vivo. RESULTS: Hsa_circ_0084927 and TPD52 were upregulated while miR-634 was downregulated in CC tissues and cells. Hsa_circ_0084927 silencing reduced tumor growth in vivo and induced cell cycle arrest, apoptosis, and curbed proliferation, colony formation, migration, and invasion of CC cells in vitro. Hsa_circ_0084927 regulated TPD52 expression through sponging miR-634. MiR-634 inhibitor reversed hsa_circ_0084927 knockdown-mediated impact on the malignancy of CC cells. TPD52 elevation abolished the repressive influence of miR-634 mimics on the malignancy of CC cells. CONCLUSION: Hsa_circ_0084927 accelerated CC advancement via upregulating TPD52 via sponging miR-634, offering a new evidence to support hsa_circ_0084927 as a promising target for CC treatment.
RESUMO
Growing evidence has been demonstrated that circular RNA circ-ITCH plays an important role in the development of several cancers. However, the role of circ-ITCH in cervical cancer has not been evaluated. The aim of the present study was to investigate the biological function of circ-ITCH in cervical cancer both in vitro and in vivo. Our results showed that circ-ITCH was lowly expressed in both human cervical cancer tissues and cell lines. Overexpression of circ-ITCH in HeLa cells significantly suppressed cell proliferation, migration, and invasion. A xenograft tumor model was established to evaluate the role of circ-ITCH in vivo. The results showed that overexpression of circ-ITCH significantly inhibited tumorigenesis of cervical cancer. Mechanism investigations proved that circ-ITCH executed its tumor suppressive activity through sponging microRNA-93-5p (miR-93-5p) and regulating the expression of forkhead box K2 (FOXK2). These findings suggest that circ-ITCH may be a therapeutic target for the management of cervical cancer.
