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The deubiquitinating protein OTUD6B promotes lung adenocarcinoma progression by stabilizing RIPK1.
Yang, Miaomiao; Wei, Yujie; He, Xin; Xia, Changwei.
Afiliação
  • Yang M; Department of Nephrology, Henan Provincial Key Laboratory of Kidney Disease and Immunology, Henan Provincial Clinical Research Center for Kidney Disease, Henan Provincial People's Hospital and People's Hospital of Zhengzhou University, 7 Weiwu Road, Zhengzhou, 450053, Henan, China. 15736738997@163.c
  • Wei Y; National Engineering Laboratory for Internet Medical Systems and Applications, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, No. 1 Jianshe Road, Erqi District, Zhengzhou, 450052, Henan, China.
  • He X; Department of Clinical Laboratory, The Fifth Affiliated Hospital of Zhengzhou University, No.3 Kangfuqian Street, Erqi District, Zhengzhou, China.
  • Xia C; Heart Center of Henan Provincial People's Hospital, Central China Fuwai Hospital of Zhengzhou University, Fuwai Central China Cardiovascular Hospital and Central China Branch of National Center Fuwai Cardiovascular Diseases, Zhengzhou, China. 13523542638@163.com.
Biol Direct ; 19(1): 46, 2024 Jun 16.
Article em En | MEDLINE | ID: mdl-38880876
ABSTRACT

BACKGROUND:

There is growing evidence indicating that deubiquitinating enzymes may contribute to tumor progression and can serve as promising therapeutic targets.

METHODS:

The overexpression of deubiquitinase OTUD6B in lung adenocarcinoma (LUAD) and its adjacent tissues was analyzed by immunohistochemistry and TCGA/GO database. Survival analysis further supported OTUD6B as a potential target for LUAD treatment. We assessed the effect of OTUD6B on LUAD cell growth using cell viability assays and conducted TUNEL staining, migration, and invasion experiments to investigate the impact of OTUD6B on the apoptosis and metastasis of LUAD cells. Additionally, we established a transplanted tumor model in nude mice to validate our findings in vivo. Finally, using IP mass spectrometry and co-IP experiments, we screened and confirmed the influence of RIPK1 as a substrate of OTUD6B in LUAD.

RESULTS:

OTUD6B is highly overexpressed in human LUAD and predicts poor prognosis in LUAD patients. OTUD6B knockdown inhibited the proliferation of LUAD cells and enhanced apoptosis and inhibited metastasis in LUAD cells suppressed. A549 xenografts revealed that OTUD6B deletion can slow down tumour growth. Additionally, OTUD6B can bind to RIPK1, reduce its ubiquitination level and increase its protein stability.

CONCLUSIONS:

Our results suggest that OTUD6B is a promising clinical target for LUAD treatment and that targeting OTUD6B may constitute an effective anti-LUAD strategy.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Proteína Serina-Treonina Quinases de Interação com Receptores / Adenocarcinoma de Pulmão / Neoplasias Pulmonares Limite: Animals / Humans Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Proteína Serina-Treonina Quinases de Interação com Receptores / Adenocarcinoma de Pulmão / Neoplasias Pulmonares Limite: Animals / Humans Idioma: En Ano de publicação: 2024 Tipo de documento: Article