Bioinformatics analysis of microarray profiling identifies the mechanism of focal adhesion kinase signalling pathway in proliferation and apoptosis of breast cancer cells modulated by green tea polyphenol epigallocatechin 3-gallate. (5th September 2018)

• Record Type: Journal Article
• Authors: Luo, Xiao; Guo, Lihua; Zhang, Lirong; Hu, Yu; Shang, Dongmei; Ji, Degang
• Is Part Of: Journal of pharmacy and pharmacology. Volume 70:Number 12(2018)
• Page Start: 1606
• Page End: 1618
• Publication Date: 2018-09-05
• Subjects: bioinformatics analysis -- breast cancer -- epigallocatechin 3-gallate -- focal adhesion kinase signalling pathway; Pharmacy -- Periodicals; Pharmacology -- Periodicals; 615.1
• DOI: 10.1111/jphp.13010
• Languages: English
• ISSNs: 0022-3573

Abstract

Abstract: Objectives: This study aimed to investigate potential gene and signal pathway associated with tumour progression. Methods: Related microarray data set of breast cancer was obtained from Gene Expression Omnibus database, and differential-expressed genes (DEGs) between two control samples and two treated samples were analysed using statistical software R. We collected 50 epigallocatechin-3-gallate(EGCG)-related genes and 119 breast cancer-related genes to create a knowledge base for following pathway analysis. Key findings: A total of 502 mRNAs were identified as DEGs based on microarray analysis. Upregulated DEGs mainly enriched in nuclear nucleosome, cell adhesion, DNA packaging complex, Wnt-activated receptor activity, etc ., while the downregulated DEGs significantly enriched in ncRNA processing, mitotic nuclear division, DNA helicase activity, etc . DEGs mostly enriched in gap junction, cell cycle, oxidative phosphorylation, focal adhesion, etc . EGCG suppressed FAK signalling pathway. Furthermore, EGCG could inhibit breast cancer cell proliferation and promote apoptosis by modulating CCND1. Conclusions: Epigallocatechin 3-gallate might exert influence on breast cancer progression through inhibiting focal adhesion kinase (FAK) signalling pathway.