Key Role of TFEB Nucleus Translocation for Silver Nanoparticle‐Induced Cytoprotective Autophagy,Small

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Key Role of TFEB Nucleus Translocation for Silver Nanoparticle‐Induced Cytoprotective Autophagy
Small ( IF 13.0 ) Pub Date : 2018-02-19 , DOI: 10.1002/smll.201703711
Jun Lin ₁ , Yiming Liu ₁ , Hao Wu ₂ , Zhihai Huang ₂ , Jingfan Ma ₃ , Chang Guo ₃ , Feng Gao ₁ , Peipei Jin ₁ , Pengfei Wei ₁ , Yunjiao Zhang ₁ , Liu Liu ₁ , Rui Zhang ₁ , Longxin Qiu ₃ , Ning Gu ₂ , Longping Wen ₁

Affiliation

Transcription factor EB (TFEB) is a master regulator of autophagy and lysosomal biogenesis. Here, silver nanoparticles (Ag NPs)‐induced cytoprotective autophagy required TFEB is shown. Ag NPs‐induced nucleus translocation of TFEB through a well‐established mechanism involving dephosphorylation of TFEB at serine‐142 and serine‐211 but independent of both the mTORC1 and ERK1/2 pathways. TFEB nucleus translocation precedes autophagy induced by Ag NPs and leads to enhanced expression of autophagy‐essential genes. Knocking down the expression of TFEB attenuates the autophagy induction is demonstrated, and in the meantime, enhanced cell killing in HeLa cells treats with Ag NPs, indicating that TFEB is the key mediator for Ag NPs‐induced cytoprotective autophagy. The results pinpoint TFEB as a potential target for developing more effective Ag NPs‐based cancer therapeutics.

中文翻译：

TFEB核易位在银纳米颗粒诱导的细胞保护性自噬中的关键作用

转录因子EB（TFEB）是自噬和溶酶体生物发生的主要调节剂。此处显示了银纳米颗粒（Ag NPs）诱导的TFEB所需的细胞保护性自噬。Ag NPs通过完善的机制涉及TFEB在丝氨酸142和丝氨酸211上的去磷酸化而诱导的TFEB核易位，但不依赖于mTORC1和ERK1 / 2途径。TFEB核易位先于Ag NP诱导的自噬，并导致自噬必需基因的表达增强。事实证明，降低TFEB的表达可减弱自噬诱导作用，与此同时，用Ag NP治疗HeLa细胞时，细胞杀伤力增强，这表明TFEB是Ag NPs诱导的细胞保护性自噬的关键介体。

更新日期：2018-02-19

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