The modulatory role of low concentrations of bisphenol A on tamoxifen-induced proliferation and apoptosis in breast cancer cells.
Level 5 - mechanism / opinion, no new human data
Bench/in vitro cell line study without human data
PubMed 30467747 · doi:10.1007/s11356-018-3780-6
What was done
The authors investigated whether low concentrations (nanomolar range) of bisphenol A (BPA) alter tamoxifen (TAM)-induced cytotoxicity in breast cancer cells. They exposed estrogen receptor-positive (MCF-7) and estrogen receptor-negative (MDA-MB-231) cell lines to TAM and BPA, measuring apoptosis, G1-to-S cell cycle transition, and expression of cyclin D1, ERα, estrogen-related receptor γ (ERRγ), and coactivators PGC-1α and PGC-1β.
What was found
The abstract reports no numerical values, concentrations, or effect sizes. Qualitatively, low concentrations of BPA decreased TAM sensitivity in MCF-7 cells by suppressing apoptosis, promoting G1-to-S cell cycle transition, upregulating cyclin D1 and ERα, and increasing mRNA levels of ERRγ, PGC-1α, and PGC-1β. These effects did not occur in MDA-MB-231 cells.
Why it matters
The study outlines a potential mechanism through which environmental BPA exposure might attenuate the therapeutic efficacy of tamoxifen in ER-positive breast cancer.
Limits
This is an in vitro study limited to two cell lines with no animal or human clinical validation. The abstract lacks exact concentrations, numerical effect sizes, and statistical confidence intervals.
Cited by
- supports In laboratory settings, low-dose exposure to bisphenol A (BPA) promotes the proliferation and growth of estrogen-sensitive breast cancer cells.