We found a match
Your institution may have rights to this item. Sign in to continue.
- Title
Visceral obesity and cell cycle pathways serve as links in the association between bisphenol A exposure and breast cancer.
- Authors
Wang, Tsu-Nai; Yang, Pei-Jing; Tseng, Yu-Ting; Tsai, Yi-Shan; Kuo, Po-Lin; Chiu, Chien-Chih; Liang, Shih-Shin; Hsieh, Tsung-Hua; Hou, Ming-Feng; Tsai, Eing-Mei
- Abstract
It has been identified that bisphenol A (BPA) exposure causes developmental toxicity in breast cells. However, the exact molecular mechanisms underlying the association between exposure to BPA and breast cancer remain unclear. The aim of the present study was to investigate the BPA-regulated signaling pathways associated with the aggressiveness and the development of breast cancer. Microarray technology and functional gene set analyses were used to evaluate BPA and breast cancer-associated biomarkers and pathways in a discovery-driven manner. Using individual dataset analyses, it was indicated that two BPA-associated gene sets, the visceral obesity pathway, involved in visceral fat deposits and the metabolic syndrome, and the cell cycle pathway, involved in cyclins and cell cycle regulation, were significantly associated with a high grade of aggressiveness and the development of estrogen receptor (ER)-positive breast cancer (between P<0.05 and 0.0001). The pooled analysis indicated that the most significant pathway was G1/S checkpoint regulation, and the cyclin and cell cycle regulation pathway for BPA-associated ER-positive cancer. Cancer cell signaling pathways were associated with healthy breast cells developing into breast cancer. The visceral obesity and the cell cycle pathways were indicated to link BPA exposure to breast cancer. The results of the present study demonstrate a significant association between breast cancer and BPA-regulated gene pathways.
- Subjects
BREAST cancer; CELL cycle; CELL cycle regulation; BRCA genes; MICROARRAY technology
- Publication
Oncology Letters, 2020, Vol 20, Issue 1, p33
- ISSN
1792-1074
- Publication type
Article
- DOI
10.3892/ol.2020.11553