Department of Clinical Laboratory, The First People's Hospital of Shuangliu District, Chengdu, China.
Department of Thoracic Surgery, The First People's Hospital of Shuangliu District, Chengdu, China.
Ann Clin Lab Sci. 2023 Nov;53(6):872-880.
Estrogen may have a certain role in promoting lung cancer caused by tobacco. Our understanding of the carcinogenic effects and mechanisms of carcinogen mixture estrogen is limited and mostly relies on the findings from studying individual factors.
To test this hypothesis, an study was used to investigate the effects of 17 β-estradiol (E) on benzo[a]pyrene (Bap)-induced lung cancer cell A549 proliferation.
We first found that E was increased in serum samples from lung adenocarcinoma cancer (LUAD) patients, even to a small extent. We found that Bap could enhance colony formation ability, up-regulate proliferating cell nuclear antigen (PCNA) and B-cell lymphoma-2 (Bcl-2) expression, induce cell proliferation and inhibit apoptosis in A549 cells. E promoted these effects of Bap. Moreover, E2 and Bap co-exposure promoted lung cancer cell proliferation by activating the aryl hydrocarbon receptor (AHR)/protein kinase B (AKT)/extracellular regulated protein kinases (ERK1/2) signaling pathway. Inhibition of the AKT and ERK1/2 signaling pathways suppressed E and Bap co-exposure's effect on A549 cells proliferation and apoptosis.
Collectively, we conclude that E could promote the proliferative and antiapoptotic effects of Bap on A549 cells, and activation of the AHR/AKT/ERK1/2 pathway may be involved in this process.
雌激素可能在促进烟草引起的肺癌方面发挥一定作用。我们对致癌物混合物雌激素的致癌作用和机制的认识有限，主要依赖于对个别因素研究的结果。
为了验证这一假设，采用研究来探讨 17β-雌二醇（E）对苯并[a]芘（Bap）诱导的肺癌细胞 A549 增殖的影响。
我们首先发现，E 在肺腺癌（LUAD）患者的血清样本中增加，甚至在很小程度上也增加。我们发现 Bap 可以增强集落形成能力，上调增殖细胞核抗原（PCNA）和 B 细胞淋巴瘤-2（Bcl-2）的表达，诱导 A549 细胞增殖并抑制细胞凋亡。E 促进了 Bap 的这些作用。此外，E2 和 Bap 共同暴露通过激活芳香烃受体（AHR）/蛋白激酶 B（AKT）/细胞外调节蛋白激酶（ERK1/2）信号通路促进肺癌细胞增殖。抑制 AKT 和 ERK1/2 信号通路抑制了 E 和 Bap 共同暴露对 A549 细胞增殖和凋亡的影响。
综上所述，我们得出结论，E 可以促进 Bap 对 A549 细胞的增殖和抗凋亡作用，AHR/AKT/ERK1/2 通路的激活可能参与这一过程。
