4.5 Article

TCEB3 is Regulated by Circ-0000212/miR-140-3p Axis to Promote the Progression of Cervical Cancer

期刊

ONCOTARGETS AND THERAPY
卷 14, 期 -, 页码 2853-2865

出版社

DOVE MEDICAL PRESS LTD
DOI: 10.2147/OTT.S278710

关键词

cervical cancer; TCEB3; circ-0000212; miR-140-3p

资金

  1. Scientific research project plan of Weifang health and Family Planning Commission [wfwsjs 2018-009]

向作者/读者索取更多资源

The study demonstrated that TCEB3 was up-regulated in cervical cancer tissues and cells, and silencing TCEB3 inhibited proliferation and invasion, promoted apoptosis of cervical cancer cells. Furthermore, the regulatory role of circ-0000212/miR-140-3p axis in TCEB3 expression and cervical cancer progression was identified, providing a potential therapeutic target for cervical cancer treatment.
Background: Cervical cancer is a common female malignancy, which accounts for a large proportion of cancer-related mortality in the world. Therefore, exploring the mechanisms of cervical cancer progression and seeking new therapeutic targets are extraordinarily needful. The aim of this study was to explore the role of TCEB3 in cervical cancer progression. Methods: TCEB3 expression was detected in cervical cancer tissue and adjacent normal tissues using qRT-PCR and immunohistochemistry analysis. TCEB3 expression was measured in cells using Western blot and qRT-PCR assay. Flow cytometer, CCK-8, colony formation and transwell assays were used to detect cell apoptosis, viability, colonyforming ability and invasion of cervical cancer cells. The expression of Ki-67, MMP-2, and MMP-9 was detected using Western blot. Bioinformatics analysis was used to predict circRNA-miRNA and miRNA-mRNA interactions. RIP and luciferase reporter assay were used to determine the interaction relationship. Results: TCEB3 expression was up-regulated in both cervical cancer tissues and cells. Silencing of TCEB3 inhibited cell proliferation and invasion and promoted apoptosis of cervical cancer cells. Additionally, silencing of TCEB3 reduced the protein expression of Ki67, MMP-2, and MMP-9 of cervical cancer cells. Mechanistically, we identified that TCEB3 was directly targeted gene of miR-140-3p, and circ-0000212 acted as a sponge of miR-1403p. Moreover, TCEB3 was regulated by circ-0000212/miR-140-3p axis and played a tumor promotive role in cervical cancer. Conclusion: Silencing of TCEB3 attenuated cell proliferation and invasion and promoted apoptosis of cervical cancer cells, and this effect was regulated by circ-0000212/miR-140-3p axis. Our findings may provide a novel promising target for cervical cancer treatment.

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