miR-365 inhibits duck myoblast proliferation by targeting IGF-I via PI3K/Akt pathway

miR-365 通过 PI3K/Akt 通路靶向 IGF-I 抑制鸭成肌细胞增殖

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作者:Wenqiang Sun, Shenqiang Hu, Jiwei Hu, Shuang Yang, Bo Hu, Jiamin Qiu, Xiang Gan, Hehe Liu, Liang Li, Jiwen Wang

Abstract

miR-365 is found to be involved in cancer cell proliferation and apoptosis. However, it remains unknown if and how miR-365 plays a role in myoblast proliferation. In the present study, we found that overexpression of miR-365 can inhibit duck myoblast proliferation. To uncover the mechanism by which miR-365 inhibits duck myoblast proliferation, we showed that miR-365 can down-regulate insulin-like growth factor-I (IGF-I) by directly targeting its 3'untranslated region (UTR). Moreover, enhanced miR-365 decreased the mRNA expression of PI3K, Akt, mTOR and S6K. Importantly, the enhanced PI3K, Akt, mTOR and S6K expression by miR-365 inhibitor (anti-miR-365) was abrogated by treatment with LY294002, a PI3K inhibitor. Together, our results indicated that miR-365 may target IGF-I to inhibit duck myoblast proliferation via PI3K/Akt pathway.

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