Abstract
Estrogen has been postulated as a contributor for lung cancer development and progression. We reviewed the current knowledge about the expression and prognostic implications of the estrogen receptors (ER) in lung cancer, the effect and signaling pathway of estrogen on lung cancer, the hormone replacement therapy and lung cancer risk and survival, the mechanistic relationship between the ER and the epidermal growth factor receptor (EGFR), and the relevant clinical trials combining the ER antagonist and the EGFR antagonist, to investigate the role of estrogen in lung cancer. Estrogen and its receptor have the potential to become a prognosticator and a therapeutic target in lung cancer. On the other hand, tobacco smoking aggravates the effect of estrogen and endocrine disruptive chemicals from the environment targeting ER may well contribute to the lung carcinogenesis. They have gradually become important issues in the course of preventive medicine.
Highlights
Estrogens are steroid hormones. 17-β-Estradiol (E2) is the primary reproductive hormone synthesized in the ovary under the stimulation of the follicular stimulating hormone and the luteinizing hormone [1,2,3,4]
This review aims to summarize the current knowledge with regard to the expression and prognostic implications of the estrogen receptor (ER) in lung cancer, the effect and signaling pathway of estrogen on lung cancer, the hormone replacement therapy and lung cancer risk and survival, the mechanistic relationship between the ER and the epidermal growth factor receptor (EGFR), and the relevant clinical trials combining the ER antagonist and the EGFR antagonist, to investigate the role of estrogen in lung cancer
The following issues will focus on the non-small cell lung cancer (NSCLC), being mostly adenocarcinoma
Summary
Estrogens are steroid hormones. 17-β-Estradiol (E2) is the primary reproductive hormone synthesized in the ovary under the stimulation of the follicular stimulating hormone and the luteinizing hormone [1,2,3,4]. Estrogen receptors (ER) are consistently found in lung cancer tissues and cell lines, especially adenocarcinoma, and mostly in the form of the ERβ [18,19,20,21]. Estrogen up-regulated the OPN expression and promoted lung cancer cell migration via the ERβ activation of the MEK/ERK signaling pathway. This review aims to summarize the current knowledge with regard to the expression and prognostic implications of the ERs in lung cancer, the effect and signaling pathway of estrogen on lung cancer, the hormone replacement therapy and lung cancer risk and survival, the mechanistic relationship between the ER and the EGFR, and the relevant clinical trials combining the ER antagonist and the EGFR antagonist, to investigate the role of estrogen in lung cancer. The following issues will focus on the non-small cell lung cancer (NSCLC), being mostly adenocarcinoma
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