scholarly journals Overexpression of ubiquitin-specific protease 22 predicts poor survival in patients with early-stage non-small cell lung cancer

2012 ◽  
Vol 56 (4) ◽  
pp. 46 ◽  
Author(s):  
J. Ning ◽  
J. Zhang ◽  
W. Liu ◽  
Y. Lang ◽  
Y. Xue ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Early Stage ◽  
Small Cell ◽  
Small Cell Lung ◽  
Poor Survival ◽  
Specific Protease ◽  
Ubiquitin Specific Protease

scholarly journals Nuclear EGFR protein expression predicts poor survival in early stage non-small cell lung cancer

Lung Cancer ◽  
2013 ◽  
Vol 81 (1) ◽  
pp. 138-141 ◽  
Author(s):  
Anne M. Traynor ◽  
Tracey L. Weigel ◽  
Kurt R. Oettel ◽  
David T. Yang ◽  
Chong Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Protein Expression ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Early Stage ◽  
Small Cell ◽  
Small Cell Lung ◽  
Poor Survival

scholarly journals Overexpression of S100A13 protein is associated with tumor angiogenesis and poor survival in patients with early-stage non-small cell lung cancer

2018 ◽  
Vol 9 (9) ◽  
pp. 1136-1144 ◽  
Author(s):  
Shuncheng Miao ◽  
Tong Qiu ◽  
Yandong Zhao ◽  
Hongmei Wang ◽  
Xiao Sun ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Tumor Angiogenesis ◽  
Early Stage ◽  
Small Cell ◽  
Small Cell Lung ◽  
Poor Survival

scholarly journals miR-7 methylation as a biomarker to predict poor survival in early-stage non-small cell lung cancer patients

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Carlos Rodríguez-Antolín ◽  
Laura Felguera-Selas ◽  
Olga Pernía ◽  
Olga Vera ◽  
Isabel Esteban ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Patients ◽  
Cell Lung Cancer ◽  
Early Stage ◽  
Small Cell ◽  
Small Cell Lung ◽  
Poor Survival ◽  
Lung Cancer Patients

scholarly journals Ubiquitin-specific protease 22 is critical to in vivo angiogenesis, growth and metastasis of non-small cell lung cancer

2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Keqiang Zhang ◽  
Lu Yang ◽  
Jinhui Wang ◽  
Ting Sun ◽  
Yuming Guo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Repair Capacity ◽  
Mouse Xenograft Model ◽  
Specific Protease ◽  
Ubiquitin Specific Protease ◽  
Underlying Mechanisms

Abstract Background Loss of monoubiquitination of histone H2B (H2Bub1) was found to be associated with poor differentiation, cancer stemness, and enhanced malignancy of non-small cell lung cancer (NSCLC). Herein, we investigated the biological significance and therapeutic implications of ubiquitin-specific protease 22 (USP22), an H2Bub1 deubiquitinase, in non-small cell lung cancer (NSCLC). Methods USP22 expression and its clinical relevance were assessed in NSCLC patients. The effects of USP22 knockout on sensitivity to cisplatin and irradiation, and growth, metastasis of NSCLC xenografts, and survival of cancer-bearing mice were investigated. The underlying mechanisms of targeting USP22 were explored. Results Overexpression of USP22 was observed in 49.0% (99/202) of NSCLC tissues; higher USP22 immunostaining was found to be associated with enhanced angiogenesis and recurrence of NSCLC. Notably, USP22 knockout dramatically suppressed in vitro proliferation, colony formation; and angiogenesis, growth, metastasis of A549 and H1299 in mouse xenograft model, and significantly prolonged survival of metastatic cancer-bearing mice. Furthermore, USP22 knockout significantly impaired non-homologous DNA damage repair capacity, enhanced cisplatin and irradiation-induced apoptosis in these cells. In terms of underlying mechanisms, RNA sequencing and gene ontology enrichment analysis demonstrated that USP22 knockout significantly suppressed angiogenesis, proliferation, EMT, RAS, c-Myc pathways, concurrently enhanced oxidative phosphorylation and tight junction pathways in A549 and H1299 NSCLC cells. Immunoblot analysis confirmed that USP22 knockout upregulated E-cadherin, p16; reduced ALDH1A3, Cyclin E1, c-Myc, and attenuated activation of AKT and ERK pathways in these cells. Conclusions Our findings suggest USP22 plays critical roles in the malignancy and progression of NSCLC and provide rationales for targeting USP22, which induces broad anti-cancer activities, as a novel therapeutic strategy for NSCLC patient.

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