scholarly journals Ubiquitin‐specific protease 44 inhibits cell growth by suppressing AKT signaling in non‐small cell lung cancer

2019 ◽  
Vol 35 (9) ◽  
pp. 535-541 ◽  
Author(s):  
Yun‐Kui Zhang ◽  
Wen‐Ze Tian ◽  
Rong‐Sheng Zhang ◽  
Yu‐Jie Zhang ◽  
Hai‐Tao Ma
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Akt Signaling ◽  
Small Cell ◽  
Small Cell Lung ◽  
Specific Protease ◽  
Ubiquitin Specific Protease

NUSAP1 knockdown inhibits cell growth and metastasis of non‐small‐cell lung cancer through regulating BTG2/PI3K/Akt signaling

2019 ◽  
Vol 235 (4) ◽  
pp. 3886-3893 ◽  
Author(s):  
ZheYuan Xu ◽  
Yang Wang ◽  
Jian Xiong ◽  
FengXian Cui ◽  
Lan Wang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Akt Signaling ◽  
Small Cell ◽  
Small Cell Lung

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.

TPD7 inhibits the non-small cell lung cancer HCC827 cell growth by regulating EGFR signalling pathway

2021 ◽  
pp. 1-7
Author(s):  
Xiaoyan Zhang ◽  
Hongjun Zhang ◽  
Gangqiang Qi ◽  
Xing Gu ◽  
Yanjun Zhao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Signalling Pathway ◽  
Small Cell Lung
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