The environmental estrogen Bisphenol (A) enhances lung cancer progression in vitro and in vivo in presence of estradiol by targeting PI3k/Akt pathway.

A growing public health concern is the increased lung cancer incidence and mortality in women. Lung cancer prevalence in young non-smoking women and sex-specific disparities in clinical characteristics suggest other etiologic factors. Several studies have substantiated the pivotal role of estrogen and estrogen receptors (ER) in lung cancer initiation and progression. Therefore, investigating the impact of ubiquitous estrogen-mimicking chemicals in today's environment on lung cancer progression is pertinent. Here, we have used bisphenol A (BPA) as a representative xenoestrogen to treat human A549 lung cancer cell line. In addition to BPA, A549 cells have been treated with either pre- or post-menopausal estradiol (E2) concentrations (30 and 100 pg/mL), administered either concomitantly or cells have been pre-treated with E2 followed by BPA treatment. Cell proliferation, migration, ER expressions were measured. We have also measured the expressions of pEGFR, PI3K, p-Akt levels in response to E2 and BPA treatment. The ability of BPA to induce lung carcinogenesis has also been demonstrated in vivo in male and female Swiss Albino mice. The results obtained in this study demonstrate the involvement of BPA in lung cancer pathogenesis in vitro and in vivo. The study also showed increased lung cancer progression by BPA in presence of E2.