NDLI: Epigallocatechin-3-gallate suppresses cell proliferation and promotes apoptosis and autophagy in oral cancer SSC-4 cells

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Epigallocatechin-3-gallate suppresses cell proliferation and promotes apoptosis and autophagy in oral cancer SSC-4 cells

Content Provider	Scilit
Author	Braicu, Cornelia Irimie, Alexandra Iulia Zanoaga, Oana Gherman, Claudia Berindan-Neagoe, Ioana Campian, Radu Septimiu Pileczki, Valentina
Copyright Year	2015
Abstract	Epigallocatechin-3-gallate suppresses cell proliferation and promotes apoptosis and autophagy in oral cancer SSC-4 cells Alexandra Iulia Irimie,1 Cornelia Braicu,2 Oana Zanoaga,2 Valentina Pileczki,2,3 Claudia Gherman,2,4 Ioana Berindan-Neagoe,2,4–6 Radu Septimiu Campian7 1Department of Prosthodontics and Dental Materials, Faculty of Dental Medicine, “Iuliu Hatieganu” University of Medicine and Pharmacy, Cluj-Napoca, Romania; 2Research Center for Functional Genomics, Biomedicine and Translational Medicine, “Iuliu Hatieganu” University of Medicine and Pharmacy, Cluj-Napoca, Romania; 3Department of Analytical Chemistry, Faculty of Pharmacy, “Iuliu Hatieganu” University of Medicine and Pharmacy, Cluj-Napoca, Romania; 4Department of Functional Genomics and Experimental Pathology, The Oncology Institute “Prof Dr. Ion Chiricuta”, Cluj-Napoca, Romania; 5Department of Immunology, Faculty of Medicine, University of Medicine and Pharmacy, “Iuliu Hatieganu” University of Medicine and Pharmacy, Cluj-Napoca, Romania; 6Department of Experimental Therapeutics MD Anderson Cancer Center Houston, TX, USA; 7Department of Oral Rehabilitation, Faculty of Dental Medicine, “Iuliu Hatieganu” University of Medicine and Pharmacy, Cluj-Napoca, Romania Epigallocatechin-3-gallate (EGCG) is the major bioactive component of green tea. Our experimental data indicated that EGCG treatment suppresses cell proliferation of SSC-4 human oral squamous cell carcinoma (OSCC), the effect being dose- and time-dependent. In parallel was observed the activation of apoptosis and autophagy, in response to EGCG exposure in SSC-4 cells. Treatment with EGCG activates the expression of the BAD, BAK, FAS, IGF1R, WNT11, and ZEB1 genes and inhibits CASP8, MYC, and TP53. All of these results suggest that EGCG has an excellent potential to become a therapeutic compound for patients with OSCC, by inducing tumor cell death via apoptosis and autophagy. Keywords: oral squamous carcinoma, time dependent cell proliferation, gene expression
Related Links	https://www.dovepress.com/getfile.php?fileID=23865 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4346003/pdf
ISSN	11786930
DOI	10.2147/OTT.S78358
Journal	OncoTargets and therapy
Volume Number	8
Language	English
Publisher	Informa UK Limited
Publisher Date	2015-02-01
Access Restriction	Open
Subject Keyword	Journal: Oncotargets and Therapy Biochemistry and Molecular Biology Dentistry and Oral Surgery Gene Expression Oral Squamous Carcinoma Time Dependent Cell Proliferation
Content Type	Text
Resource Type	Article
Subject	Pharmacology (medical) Oncology

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