Regulation of Id1 expression by epigallocatechin‑3‑gallate and its effect on the proliferation and apoptosis of poorly differentiated AGS gastric cancer cells

Ma,Jun; Shi,Min; Li,Guangming; Wang,Na; Wei,Jue; Wang,Ting; Ma,Jiali; Wang,Yugang

doi:10.3892/ijo.2013.2043

Regulation of Id1 expression by epigallocatechin‑3‑gallate and its effect on the proliferation and apoptosis of poorly differentiated AGS gastric cancer cells

Authors:
- Jun Ma
- Min Shi
- Guangming Li
- Na Wang
- Jue Wei
- Ting Wang
- Jiali Ma
- Yugang Wang
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Affiliations: Department of Geriatrics, Shanghai Changning Central Hospital, Shanghai 200336, P.R. China, Department of Gastroenterology, Shanghai Changning Central Hospital, Shanghai 200336, P.R. China, Department of Gastroenterology, Xinhua Hospital, Shanghai Second Medical University, Shanghai 200092, P.R. China
Published online on: July 30, 2013 https://doi.org/10.3892/ijo.2013.2043
Pages: 1052-1058
Copyright: © Ma et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].

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Abstract

We investigated the inhibition of apoptosis and proliferation of poorly differentiated AGS gastric cancer cells by epigallocatechin-3-gallate (EGCG), to establish target genes for regulation by EGCG. The proliferation and apoptosis of AGS gastric cancer cells treated with EGCG were observed by cell counting kit (CCK)-8 and flow cytometry. Differential gene expression in AGS cells treated with EGCG was screened by gene expression microarrays. Id1 gene and protein expression were determined by quantitative PCR and western blot analysis. The effect of Id1 on EGCG-induced apoptosis and cell cycle arrest of AGS cells was verified with RNAi. The proliferation and apoptosis of AGS cells treated with siRNA‑Id1 was observed by CCK-8 and flow cytometry. EGCG significantly promoted apoptosis and inhibited the proliferation of AGS cells. The Id1 gene was differentially expressed in AGS cells treated with EGCG, and Id1 mRNA and protein were downregulated in AGS cells treated with EGCG, confirmed by quantitative PCR and western blot analysis. Id1 mRNA and protein were also downregulated in AGS cells treated with siRNA-Id1. The apoptosis and proliferation of AGS cells treated with siRNA-Id1 were similar to those in cells treated with EGCG. EGCG induces apoptosis and inhibits proliferation of poorly differentiated AGS gastric cancer cells, and Id1 may be one of the target genes regulated by EGCG in cancer inhibition.

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