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首页> 外文期刊>Cellular Signalling >Endoplasmic reticulum stress inhibits cell cycle progression via induction of p27 in melanoma cells
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Endoplasmic reticulum stress inhibits cell cycle progression via induction of p27 in melanoma cells

机译：内质网应激通过诱导黑色素瘤细胞中的p27抑制细胞周期进程

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摘要

The accumulation of unfolded proteins in the endoplasmic reticulum (ER) triggers the unfolded protein response (UPR), a stress signaling pathway. The UPR coordinates the induction of ER chaperones with decreased protein synthesis and growth arrest in G1 phase of the cell cycle. However, the molecular mechanism underlying UPR-induced G1 cell cycle arrest remains largely unknown. Here we report that activation of the UPR response by tunicamycin (TM), an ER stress inducer, leads to accumulation of p27 and G1 cell cycle arrest in melanoma cells. This accumulation of p27 is due to the inhibition on its polyubiquitination and subsequent degradation upon TM treatment. Correlated with p27 stabilization, the levels of Skp2, an E3 ligase for p27, are decreased in response to TM treatment. More importantly, knockdown of p27 greatly reduces TM-induced G1 cell cycle arrest. Taken together, these data implicate p27 as a critical mediator of ER stress-induced growth arrest.
机译：内质网（ER）中未折叠蛋白的积累触发了未折叠蛋白应答（UPR），这是一种应力信号传导途径。 UPR协调ER分子伴侣的诱导与细胞周期G1期的蛋白质合成减少和生长停滞。但是，UPR诱导的G1细胞周期停滞的分子机制仍然未知。在这里，我们报告说，内质网应激诱导剂衣霉素（UP）激活UPR反应导致黑色素瘤细胞中p27和G1细胞周期停滞的积累。 p27的这种积累归因于其多泛素化的抑制和随后在TM处理后的降解。与p27稳定相关，Skp2（一种针对p27的E3连接酶）的水平因TM处理而降低。更重要的是，敲除p27大大降低了TM诱导的G1细胞周期停滞。综上所述，这些数据表明p27是ER应激诱导的生长停滞的关键介质。

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