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[1]赵帅,冯玉梅.GATA3与FOXA1在luminal亚型乳腺癌细胞中相互作用的研究[J].天津医科大学学报,2024,30(05):399-404.[doi:10.20135/j.issn.1006-8147.2024.05.0399]
　ZHAO Shuai,FENG Yumei.Study on the interaction between GATA3 and FOXA1 in luminal subtype breast cancer cells[J].Journal of Tianjin Medical University,2024,30(05):399-404.[doi:10.20135/j.issn.1006-8147.2024.05.0399]
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GATA3与FOXA1在luminal亚型乳腺癌细胞中相互作用的研究(PDF)
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《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:
30卷
期数:
2024年05期
页码:
399-404
栏目:
肿瘤疾病专题
出版日期:
2024-09-25

文章信息/Info

Title:
Study on the interaction between GATA3 and FOXA1 in luminal subtype breast cancer cells
文章编号:
1006-8147（2024）05-0399-06
作者:
赵帅; 冯玉梅
（天津医科大学肿瘤医院肿瘤研究所生物化学与分子生物学研究室；乳腺癌防治教育部重点实验室；天津市恶性肿瘤临床医学研究中心；国家恶性肿瘤临床医学研究中心，天津300060）
Author(s):
ZHAO Shuai; FENG Yumei
（Department of Biochemistry and Molecular Biology，Cancer Institute and Hospital，Tianjin Medical University；Key Laboratory of Breast Cancer Prevention and Therapy，Tianjin Medical University，Ministry of Education；Tianjin′s Clinical Research Center for Cancer；National Clinical Research Center for Cancer，Tianjin 300060，China）
关键词:
luminal亚型乳腺癌; GATA3; FOXA1; 蛋白质相互作用
Keywords:
luminal subtype breast cancer; GATA3; FOXA1; protein interaction
分类号:
R737.9
DOI:
10.20135/j.issn.1006-8147.2024.05.0399
文献标志码:
A
摘要:
目的：探讨GATA3与FOXA1在luminal亚型乳腺癌细胞中的相互作用。方法：基于cBioportal For Cancer Genomics公共数据库中乳腺癌临床病例数据集，分析luminal A、luminal B和basal-like亚型乳腺癌组织中GATA3与FOXA1mRNA表达水平的相关性；利用蛋白-蛋白相互作用数据库STRING和分析工具Cytoscape预测GATA3与FOXA1的相互作用。以luminal亚型的MCF-7和T-47D乳腺癌细胞以及basal-like亚型的MDA-MB-231和SUM-149PT乳腺癌细胞为研究对象，采用RT-qPCR和Western印迹检测GATA3和FOXA1的mRNA和蛋白表达水平；细胞免疫荧光检测GATA3和FOXA1的细胞定位；蛋白质免疫共沉淀验证GATA3与FOXA1之间的相互作用。结果：临床病例数据分析显示GATA3与FOXA1在luminal A、luminal B和basal-like亚型乳腺癌组织中mRNA的表达均呈正相关（r=0.404 7、0.476 1、0.587 6，均P<0.000 1）。蛋白质相互作用预测显示GATA3与FOXA1存在潜在的相互作用关系。Luminal乳腺癌细胞中GATA3和FOXA1的mRNA（t=80.95、79.73、33.84、33.60，均P<0.000 1；t=15.24、5.21、14.95、14.93，均P<0.001）和蛋白（t=29.63、28.48、36.60、35.60，均P<0.000 1；t=34.06、35.30、75.01、74.32，均P<0.000 1）表达水平显著高于basal-like细胞。GATA3与FOXA1在MCF-7和T-47D细胞核中共定位。GATA3与FOXA1存在蛋白相互作用。结论：GATA3与FOXA1可能通过相互作用维持luminal亚型乳腺癌表型稳态，抑制肿瘤恶性进展。
Abstract:
Objective：To investigate the mutual interaction between GATA3 and FOXA1 in luminal subtype breast cancer cells. Methods：The correlation between GATA3 and FOXA1mRNA expression levels in luminal A，luminal B，and basal-like subtypes of breast cancer was analyzed based on the dataset of breast cancer clinical cases in the cBioPortal for Cancer Genomics public database.The interaction of GATA3 and FOXA1 was predicted using the protein-protein interaction database STRING and the analysis tool Cytoscape. The mRNA and protein expression levels of GATA3 and FOXA1 were detected by RT-qPCR and Western blotting in luminal subtype breast cancer MCF-7 and T-47D cells，as well as basal-like subtype breast cancer MDA-MB-231 and SUM-149PT cells as the study subjects.Cellular localization of GATA3 and FOXA1 was detected by immunofluorescence staining.The mutual interaction between GATA3 and FOXA1 validated by protein immunoprecipitation. Results：The analysis of clinical case data showed that the mRNA expression of GATA3 was positively correlated with that of FOXA1 in luminal A，luminal B and basal-like subtypes of breast cancer tissues（r=0.404 7，0.476 1，0.587 6，all P<0.000 1）. The protein-protein interaction database prediction indicated a potential interaction between GATA3 and FOXA1. The mRNA（t=80.95，79.73，33.84，33.60，all P<0.000 1；t=15.24，15.21，14.95，14.93，all P<0.001）and protein（t=29.63，28.48，36.60， 35.60，all P<0.000 1；t=34.06，35.30，75.01，74.32，all P<0.000 1）expression levels of GATA3 and FOXA1 were significantly higher in luminal breast cancer cells than those in basal-like cells. GATA3 and FOXA1 were co-localizedin the nuclei of MCF-7 and T-47D cells. GATA3 was interacted with FOXA1. Conclusion：GATA3 and FOXA1 may maintain the homeostasis of luminal subtypes in breast cancer cells and inhibit tumor aggressive progression through mutual interaction.

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备注/Memo

备注/Memo:
基金项目 天津市医学重点学科（专科）建设项目（TJYXZDXK-009A）
作者简介 赵帅（1997-），男，硕士在读，研究方向：肿瘤分子生物学；
通信作者：冯玉梅，E-mail：ymfeng@tmu.edu.cn。
更新日期/Last Update: 2024-09-20