Lung cancer has been one of the major cancers leading to mortalities worldwide. In addition to smoking, estrogen is considered to play an important role in the lung cancer development because women have a higher proportion of adenocarcinoma than men. In the environment, there are many metabolites and waste products that mimic human estrogen structurally and functionally. 17α-Ethynylestradiol (EE2) which is used as an oral contraceptive is released into wastewater after being utilized. Moreover, 4-nonylphenol (NP) which is found in the petrochemical products and air pollutants reveals estrogenic activity. In the present study, 17β-estradiol (E2), EE2, and NP are administered to stimulate male lung adenocarcinoma cells (A549) and female lung adenocarcinoma cells (H1435). The results demonstrate that EE2 and NP stimulate A549 and H1435 cells proliferation in a dose- and time-dependent manner. Both estrogen receptors α and β are simultaneously activated. In response to estrogens, up-regulation of the epidermal growth factor receptor and extracellular signal-regulated kinase expression occurs. In conclusion, this is the first study to report that EE2 and NP exert a biotoxic effect to stimulate the proliferation of both male and female lung cancer cell in a dose- and time- dependent manner. The environmental hormones posing new challenges for lung cancer deserve further investigation.
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| http://dx.doi.org/10.1016/j.chemosphere.2018.11.123 | DOI Listing |
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