4.4 Article

Hsa_circ_0084912 Drives the Progression of Cervical Cancer Via Regulating miR-429/SOX2 Pathway

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MOLECULAR BIOTECHNOLOGY
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DOI: 10.1007/s12033-023-00701-6

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circRNA; miRNA; mRNA; Cervical carcinoma

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This study focuses on the role of hsa_circ_0084912 in cervical cancer (CC) and its molecular pathways. The expression of Hsa_circ_0084912, miR-429, and SOX2 in CC tissues and cells was determined using Western blotting and qRT-PCR. Functional assays including CCK-8, colony formation, Transwell, and xenograft tumor model were performed to analyze the effects of hsa_circ_0084912 on CC cell proliferation, migration, and tumor growth. It was found that hsa_circ_0084912 promoted CC cell malignancies by sponging miR-429 to control SOX2 expression.
We focus on hsa_circ_0084912's role in Cervical cancer (CC) and its molecular pathways. In order to determine the expression of Hsa_circ_0084912, miR-429, and SOX2 in CC tissues and cells, Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) were utilized. Cell counting kit 8 (CCK-8), colony formation and Transwell assays were respectively to analyze CC cell proliferation viability, clone formation ability and migration. RNA immunoprecipitation (RIP) assay and dual-luciferase assay were used to assure the targeting correlation among hsa_circ_0084912/SOX2 and miR-429. By using a xenograft tumor model, the hsa_circ_0084912 impact on CC cell proliferation in vivo was confirmed. Hsa_circ_0084912 and SOX2 expressions were aggrandized, however, miR-429 expression was descended in CC tissues and cells. Silencing hsa_circ_0084912 inhibited cell proliferation, colony formation and migration in vitro of CC, meanwhile reducing growth of tumor in vivo. MiR-429 might be sponged by Hsa_circ_0084912 to control SOX2 expression. Hsa_circ_0084912 knockdown impact on the malignant phenotypes of CC cells was restored by miR-429 inhibitor. Moreover, SOX2 silencing eliminated the promotive effects of miR-429 inhibitors on CC cell malignancies. By raising SOX2 expression by targeting miR-429, hsa_circ_0084912 accelerated the development of CC, offering fresh proof that it is a viable target for CC treatment.

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