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

被引：11

作者：

Sun, Wenqiang ^{[1
]}

Hu, Shenqiang ^{[1
]}

Hu, Jiwei ^{[1
]}

Yang, Shuang ^{[1
]}

Hu, Bo ^{[1
]}

Qiu, Jiamin ^{[1
]}

Gan, Xiang ^{[1
]}

Liu, Hehe ^{[1
]}

Li, Liang ^{[1
]}

Wang, Jiwen ^{[1
]}

机构：

[1] Sichuan Agr Univ, Farm Anim Genet Resources Explorat & Innovat Key, Yaan 625014, Sichuan, Peoples R China

来源：

BIOSCIENCE REPORTS | 2019年 / 39卷

关键词：

MUSCLE; EXPRESSION; MICRORNAS; GROWTH; DIFFERENTIATION; APOPTOSIS; MIR-206; CELLS;

D O I：

10.1042/BSR20190295

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页数：12

共 30 条

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