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MicroRNA-148a-3p inhibits the proliferation of cervical cancer cells by regulating the expression levels of DNMT1 and UTF1
MicroRNA-148a-3p inhibits the proliferation of cervical cancer cells by regulating the expression levels of DNMT1 and UTF1
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MicroRNA-148a-3p inhibits the proliferation of cervical cancer cells by regulating the expression levels of DNMT1 and UTF1
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MicroRNA-148a-3p inhibits the proliferation of cervical cancer cells by regulating the expression levels of DNMT1 and UTF1
MicroRNA-148a-3p inhibits the proliferation of cervical cancer cells by regulating the expression levels of DNMT1 and UTF1

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MicroRNA-148a-3p inhibits the proliferation of cervical cancer cells by regulating the expression levels of DNMT1 and UTF1
MicroRNA-148a-3p inhibits the proliferation of cervical cancer cells by regulating the expression levels of DNMT1 and UTF1
Journal Article

MicroRNA-148a-3p inhibits the proliferation of cervical cancer cells by regulating the expression levels of DNMT1 and UTF1

2021
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Overview
MicroRNAs (miRs) serve a key role in carcinogenesis. miR-148a-3p has been demonstrated to act as a tumor suppressor in several tumors, such as epithelial ovarian cancer and esophageal cancer. However, to the best of our knowledge, the role of miR-148a-3p in cervical cancer remains unclear. In the present study, the expression levels of miR-148a-3p measured by reverse transcription-quantitative PCR were significantly decreased in cervical cancer tissues compared with that in normal cervical tissues. Furthermore, overexpression of miR-148a-3p markedly suppressed the proliferation of cervical cancer cells. The luciferase reporter assay demonstrated that DNA methyltransferase 1 (DNMT1) was the target gene of miR-148a-3p and that its expression measured by western blotting was inhibited by miR-148a-3p in cervical cancer cells. Correlation analysis highlighted that the expression levels of the undifferentiated embryonic cell transcription factor-1 (UTF1) were negatively associated with the expression levels of DNMT1 in cervical cancer tissues. Furthermore, DNMT1 knockdown increased the expression of UTF1 and decreased the methylation level of UTF1 promoter. These data demonstrated the expression levels of UTF1 were regulated by DNMT1 methylation in cervical cancer cells. Collectively, the results of the present study suggested that miR-148a-3p may inhibit the proliferation of cervical cancer cells by regulating the expression levels of DNMT1/UTF1, which provides potential therapeutic targets for cervical cancer.