Document Type

Paper- Restricted to Campus Access

Publication Date


Faculty Mentor

Rebecca Roberts


Bisphenols are common plasticizers that share a similar structure to estrogen. Bisphenols can bind to estrogen receptors and disrupt both classical and non-classical pathways and elicit a cellular response. The endogenous hormone, estrogen, is known to modify enzyme function and elicit cell proliferation of certain cell types, particularly breast cancer cells. Similar effects, including an increase in metastasis, are seen in breast cancer cells exposed to bisphenol A (BPA). The activation of estrogen-based pathways has also been shown to increase cathepsin expression in cancer cells, which indicates worse prognoses and higher rates of metastasis. Although many industrial companies have removed BPA from their plastics, it is often replaced with structurally analogous bisphenols. We hypothesize that these bisphenols increase metastasis and cathepsin expression of cells due to structural similarities with estrogen, enabling binding to estrogen receptors. Using MTT assays and Western blotting, we hope to show that BPA and its structural analogs may modify the behavior of the MCF-7 model line of human breast cancer cells.


Presented as part of the Ursinus College Celebration of Student Achievement (CoSA) held April 22, 2021.

The downloadable file is a poster presentation with audio commentary with a run time of 4:34.


Available to Ursinus community only.