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Updated: Jun 6, 2026
![Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate (DMBA-TPA)](/_next/image?url=https%3A%2F%2Fcloudfront.jove.com%2FCDNSource%2Fteasers%2F60445.jpg&w=3840&q=50)
Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate (DMBA-TPA)
Published on: December 19, 2019
Polycyclic aromatic hydrocarbon derivative 3-hydroxybenz[a]anthracene promotes the progression of T47D breast cancer
Wenting Song1,2, Xiao Kang1, Xueyan Li1,2
1School of Medicine, Henan Polytechnic University, Jiaozuo, China.
Abstract:
Polycyclic aromatic hydrocarbon derivatives, as a class of environmental pollutants, often exhibit higher toxicity than their parent polycyclic aromatic hydrocarbons, posing potential health risks. This study selected the potentially estrogenic derivative 3-hydroxybenz[a]anthracene as the research subject. Using the estrogen receptor-positive breast cancer cell line T47D as a model, the effects of this compound on cell proliferation, migration, invasion, and apoptosis were evaluated through EdU staining, colony formation, scratch healing, Transwell invasion, and apoptosis assays to evaluate its effects on cell proliferation, migration, invasion, and apoptosis. Western blot analysis was employed to detect the expression of relevant signaling proteins. Results indicate that 3-hydroxybenz[a]anthracene promotes T47D cell proliferation by activating the PI3K/AKT signaling pathway, thereby upregulating AKT, p-AKT, and c-Myc protein expression. It enhances cell migration and invasion by downregulating E-Cadherin and MMP9 while simultaneously upregulating Vimentin and MMP2 protein expression. Furthermore, this compound simultaneously upregulates Bax and Bcl-2 expression, ultimately inducing apoptosis in T47D cells. This study confirms that 3-hydroxybenz[a]anthracene exhibits estrogen-like activity in vitro and can influence malignant biological behaviors of breast cancer cells by regulating relevant signaling pathways. These findings provide experimental evidence for further evaluating the endocrine-disrupting effects and breast cancer risks associated with such environmental pollutants.
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