NDLI: p,p′-Dichlorodiphenyltrichloroethane inhibits the apoptosis of colorectal adenocarcinoma DLD1 cells through PI3K/AKT and Hedgehog/Gli1 signaling pathways

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p,p′-Dichlorodiphenyltrichloroethane inhibits the apoptosis of colorectal adenocarcinoma DLD1 cells through PI3K/AKT and Hedgehog/Gli1 signaling pathways

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Toxicology Research Vol - 4 Issue - 4

Toxicology Research Vol - 4 Issue - 3

Toxicology Research Vol - 4 Issue - 2

Toxicology Research Vol - 4 Issue - 1

Toxicology Research Vol -3

Toxicology Research Vol -2

Toxicology Research Vol -1

p,p′-Dichlorodiphenyltrichloroethane inhibits the apoptosis of colorectal adenocarcinoma DLD1 cells through PI3K/AKT and Hedgehog/Gli1 signaling pathways

Content Provider	Royal Society of Chemistry (RSC)
Author	Xiao, Hong Liu, Weiping Li, Zhuoyu Song, Li Zhao, Meirong Liu, Jianxin
Copyright Year	2015
Abstract	Dichlorodiphenyltrichloroethane (DDT) is a ubiquitous organochlorine pollutant in the environment and has been associated with colorectal cancer development. The present study investigated the possible effects of p,p′-DDT on the apoptosis of colorectal adenocarcinoma cells and the relevant molecular mechanism. The results indicated that exposure to low concentrations of p,p′-DDT (10−10, 10−9 and 10−8 M) for 96 h markedly inhibited the apoptosis of human colorectal adenocarcinoma DLD1 cells induced by 5-FU. Moreover, p,p′-DDT exposure led to upregulation of Bcl-2 along with downregulation of Bax and procaspase-3 in both DLD1 cells and tumor tissue of a mouse xenograft model. We also found that activated caspase-3 activity was decreased after p,p′-DDT treatment. The addition of estrogen receptor (ER) inhibitor, ICI 182780, had no significant effect on the action of p,p′-DDT. In addition, p,p′-DDT exposure could activate PI3K/AKT and Hedgehog/Gli1 signaling cascades. Treatment with the PI3K inhibitor LY294003 or the Hedgehog/Gli1 inhibitor GANT61 prevented p,p′-DDT-induced signaling pathways of PI3K/AKT and Hedgehog/Gli1, respectively. Consistently, LY294003 or GANT61 attenuated the ability of p,p′-DDT to suppress 5-FU-induced apoptosis in DLD1 cells. Taken together, our results demonstrated that p,p′-DDT inhibited the apoptosis of human colorectal adenocarcinoma DLD1 cells by activating PI3K/AKT and Hedgehog/Gli1 signaling pathways.
Starting Page	1214
Ending Page	1224
Page Count	11
File Format	HTM / HTML PDF
ISSN	2045452X
Volume Number	4
Issue Number	5
Journal	Toxicology Research
DOI	10.1039/c5tx00006h
Language	English
Publisher	Royal Society of Chemistry
Access Restriction	Open
Subject Keyword	Bcl-2 Organochloride Estrogen receptor Protein kinase B Xenotransplantation Imperial Chemical Industries Colorectal cancer Enzyme inhibitor GLI1 Phosphoinositide 3-kinase inhibitor ICI Phosphoinositide 3-kinase Bcl-2-associated X protein Mouse DDT Bax Caspase 3 Apoptosis
Content Type	Text
Resource Type	Article
Subject	Health, Toxicology and Mutagenesis Toxicology

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p,p′-Dichlorodiphenyltrichloroethane inhibits the apoptosis of colorectal adenocarcinoma DLD1 cells through PI3K/AKT and Hedgehog/Gli1 signaling pathways

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p,p′-Dichlorodiphenyltrichloroethane inhibits the apoptosis of colorectal adenocarcinoma DLD1 cells through PI3K/AKT and Hedgehog/Gli1 signaling pathways