NDLI: (-)-Epigallocatechin-3-gallate induces cancer cell apoptosis via acetylation of amyloid precursor protein.

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(-)-Epigallocatechin-3-gallate induces cancer cell apoptosis via acetylation of amyloid precursor protein.

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(-)-Epigallocatechin-3-gallate induces cancer cell apoptosis via acetylation of amyloid precursor protein.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Hu, Qian Chang, Xiang Yan, Rong Rong, Cuiping Yang, Cong Cheng, Shuyi Gu, Xiaoqiong Yao, Herui Hou, Xueqin Mo, Yousheng Zhao, Luguang Chen, Yunbo Dinlin, Xiaoxiao Wang, Qi Fang, Shuhuan
Description	Country affiliation: China Author Affiliation: Hu Q ( Department of Oncology, Sun Yat-Sen Memorial Hospital of Sun Yat-Sen University, Guangzhou, 510120, China.)
Abstract	Epigenetic modifications are involved in cancer pathogenesis, and HDACis are considered potential therapeutic agents. We and others have shown the inhibitory activity of EGCG on HDAC1. But little is known about the effect of EGCG as on epigenetic regulation in cancer. Here, we try to demonstrate that EGCG acts as an HDACi downregulated APP expression, which was pathophysiologically upregulated in cancers and exerts a key role in cancer cell growth. We used PC-12 cells, SK-N-SH cells and primary tumor tissues for our analysis. Male 4-week-old athymic nude mice were used for heterotopic tumor growth assay. We employed Western blotting analysis to detect Bcl-2, Bax, APP, caspase-3, caspase-7, HDAC1 and H4Ac. We used AnnexinV-FITC and TUNEL staining for apoptosis detection. Tumor tissues were examined by immunohistochemical staining. We demonstrated that EGCG suppresses the growth of xenografted adrenal pheochromocytoma. Flow cytometry analysis and TUNEL staining showed that EGCG induced the apoptosis. Treatment with EGCG resulted in decrease in Bcl-2 but increase in Bax and activated caspase-3 and caspase-7. HDAC inhibitor EGCG leaded to hyperacetylated histone H4 by immunofluorescence. EGCG decreased APP levels by immunofluorescence staining and Western blot analysis. Silencing specific to HDAC1 leaded to caspase-3 and caspase-7 activation and cleavage. Our results are the first to demonstrate a functional interaction between EGCG and APP in suppression tumor growth, and provide a new epigenetic effects of EGCG on antitumor.
File Format	HTM / HTML
ISSN	13570560
Issue Number	1
Volume Number	32
e-ISSN	1559131X
Journal	Medical Oncology
Language	English
Publisher	Springer
Publisher Date	2015-01-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Immunohistochemistry Research Support, Non-u.s. Gov't Epigenesis, Genetic Humans Male In Situ Nick-end Labeling Journal Article Flow Cytometry Neoplasms, Experimental Anticarcinogenic Agents Acetylation Discipline Oncology Catechin Drug Therapy Rats Pharmacology Metabolism Drug Effects Blotting, Western Xenograft Model Antitumor Assays Pathology Animals Mice, Nude Fluorescent Antibody Technique Cell Line, Tumor Amyloid Beta-protein Precursor Histone Deacetylase Inhibitors Mice Analogs & Derivatives Apoptosis
Content Type	Text
Resource Type	Article
Subject	Hematology Cancer Research Oncology

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