Arsenic induces gender difference of estrogen receptor in AECII cells from ICR fetal mice

被引:12
作者
Che, Wangjun [1 ,2 ]
Yang, Mengping [1 ,3 ]
Cheng, Yaling [1 ]
Wu, Mei [1 ]
Lan, Yajia [1 ]
Zhang, Hao [1 ]
机构
[1] Sichuan Univ, West China Sch Publ Hlth, Dept Environm Hlth & Occupat Med, 16,Sect 3,Ren Min Nan Rd, Chengdu 610041, Sichuan, Peoples R China
[2] Kunming Ctr Dis Control & Prevent, Dept Occupat Hlth, 4 Ziyun Rd, Kunming 650228, Yunnan, Peoples R China
[3] Chongqing Ctr Dis Control & Prevent, 8 Changjiang Second Rd, Chongqing 400042, Peoples R China
基金
中国国家自然科学基金;
关键词
Mice; TypeII alveolar epithelial cells; Estrogen receptor beta; Sodium arsenite; Lung cancer; Gender difference; NF-KAPPA-B; LUNG-CANCER; RISK; EXPRESSION; BETA; EXPOSURE;
D O I
10.1016/j.tiv.2019.01.014
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
Arsenic is a confirmed human lung carcinogen with estrogenic activity. There are gender differences in the incidence of lung cancer. Estrogen receptors (ER) play an important role in the process of the development of lung cancer. In order to understand the gender difference effects of ER during carcinogenesis of lung induced by arsenic, the effects of arsenic and estrogen receptor antagonist (ICI182780) on expression levels of estrogen receptor beta (ER beta), extracellular regulated protein kinase (ERK1/2) and nuclear factor kappa B (NF-kappa B/P65) in type II alveolar epithelial cells (AECII) from different sex ICR fetal mice lung were detected. Results showed that arsenic increased the expression levels of mRNA and protein of ER beta, ERK1/2 and NF-kappa B/P65, and ICI182780 inhibited the increase. Furthermore, there remains a gender difference in these changes. To summarize, the observations here strongly suggested that estrogen receptor and its mediated signal pathway molecules might have critical roles of the gender difference of incidence of lung cancer in arsenic induced.
引用
收藏
页码:133 / 140
页数:8
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