TMEPAI increases lysosome stability and promotes autophagy
TMEPAI increases lysosome stability and promotes autophagy
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TMEPAI 增加溶酶体稳定性并促进自噬
DOI：
10.1016/j.biocel.2016.05.004
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发表时间：
2016
期刊：
影响因子：
--
通讯作者：
Aipo Diao
中科院分区：
文献类型：
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作者：
Shenheng Luo;Meng Yang;Dan Lv;Lei Jing;Yuyin Li;Zhenxing Liu;Aipo Diao
自噬正在成为正常细胞和癌细胞对环境变化的关键反应，并在细胞代谢和受损细胞器的维持中发挥重要作用。跨膜前列腺雄激素诱导蛋白（TMEPAI）是一种在肿瘤细胞中高表达的促肿瘤因子。在这项研究中，我们发现 TMEPAI 的消耗会导致溶酶体不稳定并抑制自噬。进一步的研究表明，TMEPAI耗竭诱导的自噬抑制与Beclin-1的调节有关。 TMEPAI 的消耗会增加癌细胞对化疗药物的敏感性。我们的研究揭示了 TMEPAI 在促进溶酶体稳定性和自噬中的作用，这可能用作癌症化疗的靶点。
Autophagy is emerging as a critical response of normal and cancer cells to environmental changes and plays an important role in cell metabolism and maintenance of damaged organelles. Transmembrane prostate androgen-induced protein (TMEPAI) is a pro-tumorigenic factor with high expression in tumor cells. In this study, we showed that depletion of TMEPAI leads to lysosomal labilization and inhibits autophagy. Further study showed that the inhibition of autophagy induced by the depletion of TMEPAI is involved in regulation of Beclin-1. Depletion of TMEPAI increases the sensitivity of cancer cells to chemotherapeutic drugs. Our study reveals the role of TMEPAI in promoting lysosome stability and autophagy, which might be used as a target for cancer chemotherapeutic treatment.