Suppr超能文献

[癌胚抗原相关细胞黏附分子6通过抑制上皮-间质转化抑制鼻咽癌细胞的增殖和迁移]

[CEACAM6 inhibits proliferation and migration of nasopharyngeal carcinoma cells by suppressing epithelial-mesenchymal transition].

作者信息

Tao Lu, Wei Zhuoli, Wang Yueyue, Xiang Ping

机构信息

Central Laboratory, First Affiliated Hospital of Bengbu Medical University, Bengbu 233004, China.

Anhui Provincial Key Laboratory of Basic and Translational Research on Inflammation-Related Diseases, Bengbu 233004, China.

出版信息

Nan Fang Yi Ke Da Xue Xue Bao. 2025 Mar 20;45(3):566-576. doi: 10.12122/j.issn.1673-4254.2025.03.14.

Abstract

OBJECTIVES

To investigate CEACAM6 expression in nasopharyngeal carcinoma (NPC) and its regulatory effects on tumor cell proliferation, migration, and epithelial-mesenchymal transition (EMT).

METHODS

CEACAM6 expression in NPC was analyzed using GEO datasets and validated by immunohistochemistry in NPC tissues and by Western blotting and RT-qPCR in NPC cell lines (HNE1, C666-1, HK1, 5-8F and CNE2Z) and normal nasopharyngeal epithelial NP69 cells. In the NPC cell lines, the effects of lentivirus-mediated CEACAM6 overexpression and knockdown on cell proliferation, migration, invasion and cytoskeletal structures were evaluated using CCK-8 assay, Edu staining, wound healing assay, Transwell assay, and phalloidin staining. Western blotting was performed to determine the expressions of EMT-related proteins (FN1, ITGA5, ITGB1, E-cadherin, N-cadherin and vimentin) in the NPC cells and the effect of FN1 overexpression on ITGA5 and ITGB1 protein expressions.

RESULTS

Analysis of the data from the GEO datasets suggested that CEACAM6 was significantly downregulated in NPC, which was associated with poor patient prognosis. Immunohistochemistry also showed low expressions of CEACAM6 in clinical NPC tissues (<0.05). In NPC cells, CEACAM6 overexpression significantly suppressed cell proliferation, migration and invasion and reduced the fluorescence intensity of actin. CEACAM6 overexpression also resulted in significant downregulation of FN1, ITGA5, ITGB1, N-cadherin and vimentin expressions and upregulation of E-cadherin expression, and FN1 overexpression obviously attenuated the inhibitory effect of CEACAM6 overexpression on ITGA5 and ITGB1 expressions.

CONCLUSIONS

CEACAM6 inhibits NPC cell migration and invasion by inhibiting EMT via regulating FN1, ITGA5 and ITGB1 expressions.

摘要

目的

研究癌胚抗原相关细胞黏附分子6(CEACAM6)在鼻咽癌(NPC)中的表达及其对肿瘤细胞增殖、迁移和上皮-间质转化(EMT)的调控作用。

方法

利用基因表达综合数据库(GEO)数据集分析NPC中CEACAM6的表达,并通过免疫组织化学在NPC组织中进行验证,通过蛋白质免疫印迹法(Western blotting)和逆转录-定量聚合酶链反应(RT-qPCR)在NPC细胞系(HNE1、C666-1、HK1、5-8F和CNE2Z)及正常鼻咽上皮NP69细胞中进行验证。在NPC细胞系中,使用细胞计数试剂盒-8(CCK-8)检测、5-乙炔基-2'-脱氧尿苷(Edu)染色、伤口愈合试验、Transwell试验和鬼笔环肽染色评估慢病毒介导的CEACAM6过表达和敲低对细胞增殖、迁移、侵袭和细胞骨架结构的影响。进行蛋白质免疫印迹法以确定NPC细胞中EMT相关蛋白(纤连蛋白1(FN1)、整合素α5(ITGA5)、整合素β1(ITGB1)、E-钙黏蛋白、N-钙黏蛋白和波形蛋白)的表达以及FN1过表达对ITGA5和ITGB蛋白表达的影响。

结果

对GEO数据集数据的分析表明,CEACAM6在NPC中显著下调,这与患者预后不良相关。免疫组织化学也显示临床NPC组织中CEACAM6表达较低(<0.05)。在NPC细胞中,CEACAM6过表达显著抑制细胞增殖、迁移和侵袭,并降低肌动蛋白的荧光强度。CEACAM6过表达还导致FN1、ITGA5、ITGB1、N-钙黏蛋白和波形蛋白表达显著下调以及E-钙黏蛋白表达上调,并且FN1过表达明显减弱了CEACAM6过表达对ITGA5和ITGB1表达的抑制作用。

结论

CEACAM6通过调节FN1、ITGA5和ITGB1的表达抑制EMT,从而抑制NPC细胞的迁移和侵袭。

相似文献

3
Function of AXL and molecular mechanisms in regulation of nasopharyngeal carcinoma.AXL 的功能及其对鼻咽癌的调控的分子机制。
Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2022 Jun 28;47(6):685-697. doi: 10.11817/j.issn.1672-7347.2022.210786.

本文引用的文献

7
Pharmacological targeting of netrin-1 inhibits EMT in cancer.靶向轴突导向因子 1 抑制癌症中的 EMT。
Nature. 2023 Aug;620(7973):402-408. doi: 10.1038/s41586-023-06372-2. Epub 2023 Aug 2.
8
Epithelial-Mesenchymal Transition (EMT).上皮-间质转化(EMT)。
Int J Mol Sci. 2023 Jul 13;24(14):11386. doi: 10.3390/ijms241411386.

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验