Affiliations: [a] Reproductive Medicine Center, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China | [b] Center of Reproductive Medicine, The No. 1 Hospital of Wuhan, Wuhan, Hubei, China | [c] Department of Obstetrics and Gynecology, The No. 1 Hospital of Wuhan, Wuhan, Hubei, China
Correspondence:
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Corresponding author: Xiangbing Jiang, Department of Obstetrics and Gynecology, The No. 1 Hospital of Wuhan, Zhong-Shan Road 215, Wuhan, Hubei 430022, China. Tel.: +86 27 8533 2315; E-mail: [email protected].
Abstract: As a result of metastasis and high recurrence, ovarian carcinoma (OC) is one of the most frequent gynecological carcinomas affecting women up to now. In spite of advances in OC treatments, the molecular mechanisms underlying OC progression are still needed to be deeply understood. MicroRNAs (miRNAs) with aberrant expressions are widely known to regulate target genes so as to mediate diverse biological activities of tumor cells. In the present study, we inspected the expression profile and latent mechanism of miR-3666 in OC. First of all, our research revealed the down-regulated miR-3666 in OC cells. Furthermore, miR-3666 up-regulation could repress cell proliferation and migration as well as induce cell apoptosis in OC. In addition, we unmasked that miR-3666 targeted STAT3 (signal transducer and activator of transcription 3) and further down-regulated STAT3 expression. Moreover, adenylate kinase 4 (AK4) was transcriptionally enhanced by STAT3, and then miR-3666 restrained AK4 expression by mediating STAT3. In the end, rescue experiments depicted that miR-3666 suppressed the development of OC via STAT3-mediated AK4. We uncovered that miR-3666 inhibited the tumorigenesis and even development of OC via suppressing STAT3/AK4 axis, offering a novel biomarker and therapeutic target for OC.
