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首页> 外文期刊>Cellular Signalling >Upregulation of sestrin 2 expression via JNK pathway activation contributes to autophagy induction in cancer cells
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Upregulation of sestrin 2 expression via JNK pathway activation contributes to autophagy induction in cancer cells

机译：通过JNK途径激活的sestrin 2表达上调有助于癌细胞自噬的诱导

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摘要

JNK signaling functions to induce defense mechanisms that protect organisms against a variety of different situations. The sestrin 2 gene, a p53-regulated member of the sestrins family, which lead to AMPK-dependent inhibition of TOR signaling, emerges as a novel player in autophagy induction. However, the relationship between JNK pathway, autophagy induction and sestrin 2 expression remains elusive. In the present study, we identify JNK as a regulator of autophagy in nasopharyngeal carcinoma cell lines CNE1 and CNE2 exposed to excisanin A or serum deprivation and demonstrate that activation of JNK can cause upregulation of sestrin 2 expression, which could be blocked by specific siRNAs directed against JNK1/2 or c-Jun. Chromatin immunoprecipitation and luciferase reporter analysis revealed that c-Jun was transcriptionally involved in the regulation of sestrin 2. Furthermore, knockdown of sestrin 2 by siRNAs similarly inhibited autophagy induction. Moreover, silencing the expression of autophagy related gene ATG5 or sestrin 2 significantly decreases cell death induced by excisanin A. Our results therefore identify JNK as a novel mediator of sestrin 2 expression, which plays a key role in autophagy induction following anticancer therapies in cancers.
机译：JNK信号转导功能可诱导防御机制，保护生物免受各种不同情况的侵害。 sestrin 2基因是sestrins家族中p53调控的成员，导致AMPK依赖的TOR信号抑制，以自噬诱导的新角色出现。然而，JNK途径，自噬诱导和sestrin 2表达之间的关系仍然难以捉摸。在本研究中，我们确定JNK是暴露于exisanin A或血清剥夺的鼻咽癌细胞系CNE1和CNE2中自噬的调节剂，并证明JNK的激活可引起雌二醇2表达的上调，而这可能被定向的特定siRNA阻断对抗JNK1 / 2或c-Jun。染色质的免疫沉淀和荧光素酶报告基因分析表明c-Jun在转录上参与了sestrin 2的调控。此外，siRNA抑制sestrin 2的表达同样抑制了自噬的诱导。此外，沉默自噬相关基因ATG5或sestrin 2的表达可显着降低由exisanin A诱导的细胞死亡。因此，我们的结果确定JNK为sestrin 2表达的新型介体，在癌症抗癌治疗后自噬诱导中起关键作用。

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