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Inhibition of USP2 Enhances TRAIL-Mediated Cancer Cell Death through Downregulation of Survivin.
Lee, Tak Gyeom; Woo, Seon Min; Seo, Seung Un; Kim, Shin; Park, Jong-Wook; Chang, Young-Chae; Kwon, Taeg Kyu.
Afiliación
  • Lee TG; Department of Immunology, School of Medicine, Keimyung University, Daegu 42601, Republic of Korea.
  • Woo SM; Department of Immunology, School of Medicine, Keimyung University, Daegu 42601, Republic of Korea.
  • Seo SU; Department of Immunology, School of Medicine, Keimyung University, Daegu 42601, Republic of Korea.
  • Kim S; Department of Immunology, School of Medicine, Keimyung University, Daegu 42601, Republic of Korea.
  • Park JW; Department of Immunology, School of Medicine, Keimyung University, Daegu 42601, Republic of Korea.
  • Chang YC; Research Institute of Biomedical Engineering and Department of Cell Biology, School of Medicine, Catholic University of Daegu, Daegu 42472, Republic of Korea.
  • Kwon TK; Department of Immunology, School of Medicine, Keimyung University, Daegu 42601, Republic of Korea.
Int J Mol Sci ; 24(16)2023 Aug 15.
Article en En | MEDLINE | ID: mdl-37628997
Ubiquitin-specific protease 2 (USP2) is a deubiquitinase belonging to the USPs subfamily. USP2 has been known to display various biological effects including tumorigenesis and inflammation. Therefore, we aimed to examine the sensitization effect of USP2 in TRAIL-mediated apoptosis. The pharmacological inhibitor (ML364) and siRNA targeting USP2 enhanced TNF-related apoptosis-inducing ligand (TRAIL)-induced cancer cell death, but not normal cells. Mechanistically, USP2 interacted with survivin, and ML364 degraded survivin protein expression by increasing the ubiquitination of survivin. Overexpression of survivin or USP2 significantly prevented apoptosis through cotreatment with ML364 and TRAIL, whereas a knockdown of USP2 increased sensitivity to TRAIL. Taken together, our data suggested that ML364 ubiquitylates and degrades survivin, thereby increasing the reactivity to TRAIL-mediated apoptosis in cancer cells.
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Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Ligando Inductor de Apoptosis Relacionado con TNF / Neoplasias Límite: Humans Idioma: En Revista: Int J Mol Sci Año: 2023 Tipo del documento: Article

Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Ligando Inductor de Apoptosis Relacionado con TNF / Neoplasias Límite: Humans Idioma: En Revista: Int J Mol Sci Año: 2023 Tipo del documento: Article