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Oncotarget. 2015 Sep 22;6(28):25266-80. doi: 10.18632/oncotarget.4457.

MiR-125a suppresses tumor growth, invasion and metastasis in cervical cancer by targeting STAT3.

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Department of Oncology, PLA General Hospital, Beijing, China.
Department of Oncology, 309th Hospital of PLA, Beijing, China.
Department of Medical Molecular Biology, Beijing Institute of Biotechnology, Beijing, China.
Department of Nuclear Medicine, Peking University First Hospital, Beijing, China.
Department of Endocrinology and Metablism, 264th Hospital of PLA, Shanxi, China.


MiR-125a has been characterized as a tumor suppressor in several cancers. However, the role of miR-125a in cervical cancer is unknown. In this study, we found the expression of miR-125a was downregulated in cervical cancer patients, and negatively correlated with the tumor size, FIGO stage, and preoperative metastasis. Kaplan-Meier analysis showed that miR-125a expression predicted favorable outcome for cervical cancer patients. Dual luciferase assays identified the STAT3 gene as a novel direct target of miR-125a. Functional studies showed that miR-125a overexpression significantly suppressed the growth, invasion and epithelial-mesenchymal transition (EMT) of cervical cancer cells both in vitro and in vivo via decreasing STAT3 expression. Moreover, miR-125a conferred to G2/M cell cycle arrest, accompanied by inhibition of several G2/M checkpoint proteins. Mechanistically, inactivation of miR-125a during cervical carcinogenesis was caused by HPV suppression of p53 expression. Clinically, STAT3, the expression of which, predicted poorer outcome, was inversely correlated with miR-125a in cervical cancer. These data highlight the importance of miR-125a in the cell proliferation and progression of cervical cancer, and indicate that miR-125a may be a useful therapeutic target for cervical cancer.


STAT3; cell growth; cervical cancer; metastasis; miR-125a

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