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Benzotriazole Enhances Cell Invasive Potency in Endometrial Carcinoma Through CTBP1-Mediated Epithelial-Mesenchymal Transition
Author(s) -
Yiquan Wang,
Chencheng Dai,
Cheng Zhou,
Wenqu Li,
Yujia Qian,
Juan Wen,
Yang Wang,
Bing Han,
Jingjing Ma,
Juan Xu,
Ziyi Fu,
Hongjie Ruan,
Hua Tong,
Xuemei Jia
Publication year - 2017
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000486123
Subject(s) - cancer research , viability assay , carcinoma , epithelial–mesenchymal transition , malignancy , gene silencing , biology , reverse transcription polymerase chain reaction , cell , cell growth , chemistry , cancer , gene expression , metastasis , gene , biochemistry , genetics
Benzotriazole (BTR) and its derivatives, such as intermediates and UV stabilizers, are important man-made organic chemicals found in everyday life that have been recently identified as environmental toxins and a threat to female reproductive health. Previous studies have shown that BTR could act as a carcinogen by mimicking estrogen. Environmental estrogen mimics could promote the initiation and development of female cancers, such as endometrial carcinoma, a type of estrogenic-sensitive malignancy. However, there is little information on the relationship between BTR and endometrial carcinoma. In this study, we aimed to demonstrate the biological function of BTR in endometrial carcinoma and explored the underlying mechanism.

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