SENP1 deficiency promotes ER stress-induced apoptosis by increasing XBP1 SUMOylation

Zhou Jiang Shanghai Key Laboratory for Tumor Microenvironment and Inflammation; Department of Biochemistry and Molecular Cell Biology; Shanghai Jiao Tong University School of Medicine; Shanghai, China; Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education; Shanghai Jiao Tong University School of Medicine; Shanghai, China; State Key Laboratory of Oncogenes and Related Genes in Shanghai Cancer Institute; Shanghai Jiao Tong University School of Medicine; Shanghai, China; These authors contributed equally to this work.

Qiuju Fan Shanghai Key Laboratory for Tumor Microenvironment and Inflammation; Department of Biochemistry and Molecular Cell Biology; Shanghai Jiao Tong University School of Medicine; Shanghai, China; These authors contributed equally to this work.

Zhening Zhang Shanghai Key Laboratory for Tumor Microenvironment and Inflammation; Department of Biochemistry and Molecular Cell Biology; Shanghai Jiao Tong University School of Medicine; Shanghai, China; These authors contributed equally to this work.

Yanqiong Zou Shanghai Key Laboratory for Tumor Microenvironment and Inflammation; Department of Biochemistry and Molecular Cell Biology; Shanghai Jiao Tong University School of Medicine; Shanghai, China

Rong Cai Shanghai Key Laboratory for Tumor Microenvironment and Inflammation; Department of Biochemistry and Molecular Cell Biology; Shanghai Jiao Tong University School of Medicine; Shanghai, China

Qi Wang Shanghai Key Laboratory for Tumor Microenvironment and Inflammation; Department of Biochemistry and Molecular Cell Biology; Shanghai Jiao Tong University School of Medicine; Shanghai, China

Yong Zuo Shanghai Key Laboratory for Tumor Microenvironment and Inflammation; Department of Biochemistry and Molecular Cell Biology; Shanghai Jiao Tong University School of Medicine; Shanghai, China

Jinke Cheng Shanghai Key Laboratory for Tumor Microenvironment and Inflammation; Department of Biochemistry and Molecular Cell Biology; Shanghai Jiao Tong University School of Medicine; Shanghai, China; Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education; Shanghai Jiao Tong University School of Medicine; Shanghai, China; State Key Laboratory of Oncogenes and Related Genes in Shanghai Cancer Institute; Shanghai Jiao Tong University School of Medicine; Shanghai, ChinaCorrespondence[email protected]

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Abstract

The transcription factor X box-binding protein 1 (XBP1) is a key component of the endoplasmic reticulum (ER) stress response. Recently, it has been reported that the spliced XBP1 (XBP1s), an activated XBP1 during ER stress, can be SUMOylated. Here, we identify Sentrin/SUMO-specific protease 1 (SENP1) as a specific de-SUMOylation protease for XBP1. SENP1 can increase the transcriptional activity of XBP1. In Senp1^-/- cells, the SUMOylated XBP1 is accumulated, and the expression of XBP1 target genes is downregulated in response to ER stress. Moreover, SENP1 deficiency significantly increases ER stress-induced apoptosis through accumulating XBP1 SUMOylation. These results reveal an essential function of SENP1 in ER stress response through regulating XBP1 SUMOylation.

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SENP1 deficiency promotes ER stress-induced apoptosis by increasing XBP1 SUMOylation

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SENP1 deficiency promotes ER stress-induced apoptosis by increasing XBP1 SUMOylation

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