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  • br Author contributions br Funding M E B was supported

    2021-06-08


    Author contributions
    Funding M.E.B. was supported by Research Fund #3096.
    Competing interests
    Introduction Lung cancer has become one of the most common death causes in both male and female malignant tumors (Jemal et al., 2011). Air pollution, smoking and estrogen level are known risk factors of occurrence and development of lung cancer. The incidence of lung cancer in women continues to rise while that in men is gradually declined, indicating that women are more sensitive to lung carcinogens than men. However, the cause of gender difference in lung cancer is unclear. IARC (1980) confirmed that arsenic and its compounds are one of the causes of human lung cancer in 1980. Non-occupational arsenics are mainly caused by ingesting water and foods contaminated with arsenic. Because women have obviously higher incidence of lung cancer than men among arsenic-exposed population, estrogen and its receptors have become the focus of researches on gender differences in lung cancer. Gender difference in lung cancer may be related with estrogen levels in women (Baik et al., 2010). Clinical and experimental data have also proved that estrogen and its receptors have played an important role in the occurrence, development and prognosis of lung cancer (Fucic et al., 2010; Paulus et al., 2011). Estrogen receptors including ERα and ERβ are the core components for endogenous and exogenous estrogens to exert their biological effects in the body, and play an important role in the growth and differentiation of target organs and the normal physiological functions of tissue cells. Moreover, Estrogen are one risk factor of canceration of some tissues and organs (skin, lung, bladder, and endometrial cancer (Karagas et al., 2001; IARC, 2004; Jongen et al., 2009). Nowadays, few studies have been reported on the expression level of ERβ in lung cancer tissues and SB 747651A dihydrochloride and its gender difference, and results obtained are also lack of consistency. It is agreed that estrogen receptors in normal lung tissue are mainly ERβ with little or no ERα. Compared with non-cancer tissues or cell lines, ERα was not detected in lung cancer tissues, but the level of ERβ protein expression was significantly elevated (Schwartz et al., 2005). In the lung cancer patients with positive ERβ, it is considered as a functional receptor in lung tissue, and its positive expression has a promoting effect on the occurrence and development of non-small cell lung cancer (Zeng et al., 2010). The only way to repair injured alveolar epithelial cells is the proliferation and migration of AEC II cells and its transformation to type I alveolar epithelial cells, thus making alveolar wall re- epithelialization. Kim et al. (2005) proved that mice stem cells being as the origin of lung adenocarcinoma could differentiate into AEC II cells in vitro. This result has also aroused more attentions on the role of AEC II cells in the development of lung adenocarcinoma. ERβ exerts its biological effects by mediating various signal pathways and auxiliary factors. MAPK-ERK1/2 is an important signal pathway, of which ERK1/2 is related with cell proliferation (Duhamel et al., 2012). When a subject-receptor complex enters into the cell, the signal transduction is accomplished by activating Ras factor or protein kinase C and Raf-MEK-ERK cascade reaction (Yao et al., 2014). After activation, ERK1/2 can rapidly phosphorylate target protein and enhance its activity on the one hand. On another hand, it can enter the nucleus, promote the phosphorylation of transcription factor, and regulate downstream target gene expression (Glaros et al., 2010). Therefore, the detection of ERK1/2 gene and its protein expression level can reflect whether receptors outside the nucleus perform signal transduction through ERK1/2 pathway under sodium arsenite exposure. Nuclear factor κB(NF-κB) participates in the regulation of multiple gene transcription and is closely related with tumor, inflammation and cell apoptosis (Vallabhapurapu and Karin, 2009). It has been found that estrogen can inhibit or activate NF-κB through both genomic and nongenomic signaling cascades mediated by ER receptors (Stice and Knowlton, 2008). Studies have shown that ER receptors can promote the transcriptional activity of NF-κB in ligand-dependent form in some cells. At the same time, ER receptor can also cooperate with NF-κB to increase the expression of COX-2 and inhibit cell apoptosis through non-gene pathway (Hirano et al., 2007). Detecting the expression level of P50/P65 protein can reflect whether NF-κB changes or not after sodium arsenite exposure. This can indirectly reflect changes in ERβ expression in the lung cells.