miR-92a is upregulated in cervical cancer and promotes cell proliferation and invasion by targeting FBXW7
MicroRNAs (miRNAs) are involved in the cervical carcinogenesis and progression. In this study, we investigated the role of miR-92a in progression and invasion of cervical cancer. MiR-92a was significantly upregulated in cervical cancer tissues and cell lines. Overexpression of miR-92a led to remarka...
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Veröffentlicht in: | Biochemical and biophysical research communications 2015-02, Vol.458 (1), p.63-69 |
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Zusammenfassung: | MicroRNAs (miRNAs) are involved in the cervical carcinogenesis and progression. In this study, we investigated the role of miR-92a in progression and invasion of cervical cancer. MiR-92a was significantly upregulated in cervical cancer tissues and cell lines. Overexpression of miR-92a led to remarkably enhanced proliferation by promoting cell cycle transition from G1 to S phase and significantly enhanced invasion of cervical cancer cells, while its knockdown significantly reversed these cellular events. Bioinformatics analysis suggested F-box and WD repeat domain-containing 7 (FBXW7) as a novel target of miR-92a, and miR-92a suppressed the expression level of FBXW7 mRNA by direct binding to its 3′-untranslated region (3′UTR). Expression of miR-92a was negatively correlated with FBXW7 in cervical cancer tissues. Furthermore, Silencing of FBXW7 counteracted the effects of miR-92a suppression, while its overexpression reversed oncogenic effects of miR-92a. Together, these findings indicate that miR-92a acts as an onco-miRNA and may contribute to the progression and invasion of cervical cancer, suggesting miR-92a as a potential novel diagnostic and therapeutic target of cervical cancer.
•miR-92a is elevated in cervical cancer tissues and cell lines.•miR-92a promotes cervical cancer cell proliferation, cell cycle transition from G1 to S phase and invasion.•FBXW7 is a direct target of miR-92a.•FBXW7 counteracts the oncogenic effects of miR-92a on cervical cancer cells. |
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ISSN: | 0006-291X 1090-2104 |
DOI: | 10.1016/j.bbrc.2015.01.066 |