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Open Access Upregulation of MicroRNA-4262 Targets Kaiso (ZBTB33) to Inhibit the Proliferation and EMT of Cervical Cancer Cells

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More and more studies have reported that dysregulation of microRNAs (miRNAs) leads to the proliferation and EMT of multiple cancers. Recently, several reports have demonstrated that dysregulation of miR-4262 occurs in numerous cancers. However, its role and precise mechanism in human cervical cancer (CC) have not been well clarified. Hence, this study aimed to explore the biological roles and precise mechanisms of miR-4262 in CC cell lines. The level of miR-4262 was found to be significantly decreased in CC tissues and cell lines. Moreover, decreased expression of miR-4262 was closely related to increased expression of Kaiso (ZBTB33), which belongs to the BTB/POZ family, in CC tissues and cell lines. The proliferation and EMT of CC cells were inhibited by a miR-4262 mimic. However, downregulation of miR-4262 enhanced the proliferation and EMT of CC cells. Next, bioinformatics analysis predicted that miR-4262 might directly target the Kaiso gene. Besides, luciferase reporter assay had confirmed this result. Moreover, introduction of Kaiso in CC cells partially blocked the effects of miR-4262 mimic. In conclusion, miR-4262 suppressed the proliferation and EMT of CC cells by directly downregulating Kaiso.
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Keywords: Cervical cancer (CC); Epithelial‐mesenchymal transition (EMT); Kaiso; MicroRNA-4262; Proliferation

Document Type: Research Article

Affiliations: Department of Gynecology, Cangzhou Central Hospital, Hebei, P.R. China

Publication date: September 14, 2018

This article was made available online on August 11, 2017 as a Fast Track article with title: "Upregulation of MicroRNA-4262 Targets Kaiso (ZBTB33) to Inhibit the Proliferation and EMT of Cervical Cancer Cells".

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  • Formerly: Oncology Research Incorporating Anti-Cancer Drug Design
    Oncology Research Featuring Preclinical and Clincal Cancer Therapeutics publishes research of the highest quality that contributes to an understanding of cancer in areas of molecular biology, cell biology, biochemistry, biophysics, genetics, biology, endocrinology, and immunology, as well as studies on the mechanism of action of carcinogens and therapeutic agents, reports dealing with cancer prevention and epidemiology, and clinical trials delineating effective new therapeutic regimens.

    From Volume 23, Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics is Open Access under the terms of the Creative Commons CC BY-NC-ND license.

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