{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T22:52:24Z","timestamp":1784587944747,"version":"3.55.0"},"reference-count":28,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2017,8,17]],"date-time":"2017-08-17T00:00:00Z","timestamp":1502928000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cell Biology International"],"published-print":{"date-parts":[[2017,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:label\/><jats:p>A previous study has shown that microRNA\u2010708 (miR\u2010708) functions as a metastasis suppressor in ovarian cancer. In this study, we aimed to explore its implication in regulating cisplatin sensitivity in ovarian cancer cells. To this end, ovarian cancer cells were transfected with miR\u2010708\u2010expressing plasmids or vector before treatment with different concentrations of cisplatin for 48\u2009h. The 50% inhibitory concentration (IC<jats:sub>50<\/jats:sub>) value was calculated. Apoptosis was analyzed by measuring caspase\u20103 activity. The target gene mediating the function of miR\u2010708 was identified. Ectopic expression of miR\u2010708 sensitized SKOV3 and A2780 cells to cisplatin, decreasing the IC<jats:sub>50<\/jats:sub> value by two\u2010 to threefold. miR\u2010708 overexpression significantly augmented cisplatin\u2010induced apoptosis in ovarian cancer cells, which was coupled with increased caspase\u20103 activity by two\u2010 to fourfold. Similarly, overexpression of miR\u2010708 increased the sensitivity of cisplatin\u2010resistant SKOV3\/DDP and A2780\/DDP cells to cisplatin\u2010induced toxicity, reducing the IC<jats:sub>50<\/jats:sub> by three\u2010 and fivefold, respectively. Delivery of miR\u2010708 enhanced cisplatin\u2010induced elevation in caspase\u20103 activity in both cisplatin\u2010resistant and parental ovarian cancer cells. Mechanistically, miR\u2010708 downregulated the expression of insulin\u2010like growth factor 2 mRNA\u2010binding protein 1 (IGF2BP1) and suppressed Akt phosphorylation. Silencing of IGF2BP1 markedly blocked the phosphorylation of Akt. Overexpression of IGF2BP1 restored cisplatin resistance and Akt phosphorylation in miR\u2010708\u2010overexpressing ovarian cancer cells. Collectively, miR\u2010708 increases the susceptibility of ovarian cancer cells to cisplatin by targeting IGF2BP1 and inhibiting Akt signaling. Delivery of miR\u2010708 may represent a promising strategy for improving cisplatin chemotherapy.<\/jats:p><\/jats:sec>","DOI":"10.1002\/cbin.10819","type":"journal-article","created":{"date-parts":[[2017,7,7]],"date-time":"2017-07-07T13:04:54Z","timestamp":1499432694000},"page":"1110-1118","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":29,"title":["Restoration of microRNA\u2010708 sensitizes ovarian cancer cells to cisplatin via IGF2BP1\/Akt pathway"],"prefix":"10.1002","volume":"41","author":[{"given":"Xuying","family":"Qin","sequence":"first","affiliation":[{"name":"Department of Obstetrics and Gynecology Liaocheng People's Hospital Liaocheng People's Republic of China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Linlin","family":"Sun","sequence":"additional","affiliation":[{"name":"Department of Obstetrics and Gynecology Liaocheng People's Hospital Liaocheng People's Republic of 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