Adenylate Cyclase-Associated Protein 1 Is Associated With Metastasis of Non-small Cell Lung Cancer Especially in Brain Metastasis Patients and Promotes the Lung Cancer Cell Proliferation and Migration In Vitro as Well as Its Growth and Metastasis In Vivo By the Signaling Pathways of Limk1-Cofilin

CHEST Journal ◽  
2016 ◽  
Vol 149 (4) ◽  
pp. A324
Author(s):  
Changhui Wang ◽  
Shuanshuan Xie ◽  
Xiaolian Song ◽  
Min Tan
Keyword(s):  
Lung Cancer ◽  
Small Cell ◽  
Cancer Cell Proliferation ◽  
Lung Cancer Cell ◽  
Small Cell Lung ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals CEACAM5 stimulates the progression of non-small-cell lung cancer by promoting cell proliferation and migration

2020 ◽  
Vol 48 (9) ◽  
pp. 030006052095947
Author(s):  
Xinwen Zhang ◽  
Xingbao Han ◽  
Pengli Zuo ◽  
Xiuying Zhang ◽  
Hongbang Xu
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Small Cell ◽  
Clinicopathological Features ◽  
Small Cell Lung ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Human Nsclc ◽  
Proliferation And Migration

Objective To detect the expression of CEA-related cell adhesion molecule 5 (CEACAM5) in non-small-cell lung cancer (NSCLC) and explore its function in the progression and development of NSCLC. Methods qRT-PCR and immunohistochemistry were performed to detect CEACAM5 expression in human NSCLC tissues and cell lines. The correlation between CEACAM5 expression and the clinicopathological features of patients with NSCLC was also investigated. MTT, colony formation, wound healing, and immunoblot assays were performed to detect the functions of CEACAM5 in NSCLC cells in vitro, and immunoblotting was used to detect the effects of CEACAM5 on p38–Smad2/3 signaling. Results CEACAM5 expression was elevated in human NSCLC tissues and cells. We further found that CEACAM expression was correlated with clinicopathological features including T division, lymph invasion, and histological grade in patients with NSCLC. The in vitro assays confirmed that CEACAM5 depletion inhibited the proliferation and migration of NSCLC cells by activating p38–Smad2/3 signaling. We verified the involvement of CEACAM5 in the suppression of NSCLC tumor growth in mice. Conclusion CEACAM5 stimulated the progression of NSCLC by promoting cell proliferation and migration in vitro and in vivo. CEACAM5 may serve as a potential therapeutic target for the treatment of NSCLC.

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