Anoctamin 6 regulates C2C12 myoblast proliferation.
Anoctamin 6 regulates C2C12 myoblast proliferation.
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DOI：
10.1371/journal.pone.0092749
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Han R
中科院分区：
文献类型：
--
作者：
Zhao P;Torcaso A;Mariano A;Xu L;Mohsin S;Zhao L;Han R
Anoctamin 6（Ano 6）属于保守基因家族（TMEM 16），编码8种跨膜蛋白，具有Ca 2+激活的氯离子通道（CaCC）活性。最近的研究表明，ANO 6的破坏导致血液凝固缺陷和骨骼发育受损。然而，其在骨骼肌细胞中的功能仍有待确定。通过使用RNA干扰介导的（RNAi）功能丧失的方法，我们表明，Ano 6调节C2 C12成肌细胞增殖。Ano 6在C2 C12成肌细胞中高度表达，并且其表达在分化时降低。敲低Ano 6显著降低C2 C12成肌细胞增殖，但对分化的影响极小。Ano 6缺陷显著降低ERK/AKT磷酸化，其已被证明参与另一Anoctamin成员对癌细胞增殖的调节。总之，我们的数据首次证明Ano 6在C2 C12成肌细胞增殖中起着重要作用，可能通过调节ERK/AKT信号通路。
Anoctamin 6 (Ano6) belongs to a conserved gene family (TMEM16) predicted to code for eight transmembrane proteins with putative Ca2+-activated chloride channel (CaCC) activity. Recent work revealed that disruption of ANO6 leads to a blood coagulation defect and impaired skeletal development. However, its function in skeletal muscle cells remains to be determined. By using a RNA interference mediated (RNAi) loss-of-function approach, we show that Ano6 regulates C2C12 myoblast proliferation. Ano6 is highly expressed in C2C12 myoblasts and its expression decreases upon differentiation. Knocking down Ano6 significantly reduces C2C12 myoblast proliferation but has minimal effect on differentiation. Ano6 deficiency significantly reduces ERK/AKT phosphorylation, which has been shown to be involved in regulation of cancer cell proliferation by another Anoctamin member. Taken together, our data demonstrate for the first time that Ano6 plays an essential role in C2C12 myoblast proliferation, likely via regulating the ERK/AKT signaling pathway.
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DOI：
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发表时间：
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影响因子：
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