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癌胚抗原相关细胞黏附分子5通过促进细胞增殖和迁移来刺激非小细胞肺癌的进展。

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

作者信息

Zhang Xinwen, Han Xingbao, Zuo Pengli, Zhang Xiuying, Xu Hongbang

机构信息

Department of General Practice, Linyi Central Hospital, Linyi, China.

Department of Urology, Linyi Central Hospital, Linyi, China.

出版信息

J Int Med Res. 2020 Sep;48(9):300060520959478. doi: 10.1177/0300060520959478.

DOI:10.1177/0300060520959478
PMID:32993395
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7536504/
Abstract

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 , 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 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 and . CEACAM5 may serve as a potential therapeutic target for the treatment of NSCLC.

摘要

目的

检测非小细胞肺癌(NSCLC)中癌胚抗原相关细胞黏附分子5(CEACAM5)的表达,并探讨其在NSCLC进展和发展中的作用。

方法

采用qRT-PCR和免疫组织化学方法检测人NSCLC组织和细胞系中CEACAM5的表达。还研究了CEACAM5表达与NSCLC患者临床病理特征之间的相关性。进行MTT、集落形成、伤口愈合和免疫印迹分析以检测CEACAM5在NSCLC细胞中的功能,并使用免疫印迹检测CEACAM5对p38-Smad2/3信号传导的影响。

结果

CEACAM5在人NSCLC组织和细胞中表达升高。我们进一步发现CEACAM表达与NSCLC患者的临床病理特征相关,包括T分期、淋巴浸润和组织学分级。实验证实,CEACAM5缺失通过激活p38-Smad2/3信号传导抑制NSCLC细胞的增殖和迁移。我们验证了CEACAM5参与抑制小鼠NSCLC肿瘤生长。

结论

CEACAM5通过促进细胞增殖和迁移促进NSCLC的进展。CEACAM5可能作为治疗NSCLC的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61ad/7536504/54aaf44cd602/10.1177_0300060520959478-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61ad/7536504/82aef7acc85c/10.1177_0300060520959478-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61ad/7536504/728584e30d6c/10.1177_0300060520959478-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61ad/7536504/0a8c14c3c872/10.1177_0300060520959478-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61ad/7536504/423767c665d1/10.1177_0300060520959478-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61ad/7536504/54aaf44cd602/10.1177_0300060520959478-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61ad/7536504/82aef7acc85c/10.1177_0300060520959478-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61ad/7536504/728584e30d6c/10.1177_0300060520959478-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61ad/7536504/0a8c14c3c872/10.1177_0300060520959478-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61ad/7536504/423767c665d1/10.1177_0300060520959478-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61ad/7536504/54aaf44cd602/10.1177_0300060520959478-fig5.jpg

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