4.6 Article

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

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BIOSCIENCE REPORTS
卷 39, 期 -, 页码 -

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PORTLAND PRESS LTD
DOI: 10.1042/BSR20190295

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  1. Key Technology Support Program of Sichuan Province [2016NYZ0044]
  2. Project of National Science and Technology Plan for the Rural Development in China [2015BAD03B06]

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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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