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      Estrogen, Estrogen Receptor and Lung Cancer

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          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.

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          Most cited references128

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          Estrogen receptors alpha (ERα) and beta (ERβ): subtype-selective ligands and clinical potential.

          Estrogen receptors alpha (ERα) and beta (ERβ) are nuclear transcription factors that are involved in the regulation of many complex physiological processes in humans. Modulation of these receptors by prospective therapeutic agents is currently being considered for prevention and treatment of a wide variety of pathological conditions, such as, cancer, metabolic and cardiovascular diseases, neurodegeneration, inflammation, and osteoporosis. This review provides an overview and update of compounds that have been recently reported as modulators of ERs, with a particular focus on their potential clinical applications. Copyright © 2014 Elsevier Ltd. All rights reserved.
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            Cancer statistics, 1999

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              ER beta: identification and characterization of a novel human estrogen receptor.

              A novel estrogen receptor (hereinafter referred to as ER beta) was cloned using degenerate PCR primers. A comparison of the amino acid sequence of ER beta with the "classical' ER (ER alpha) shows a high degree of conservation of the DNA-binding domain (96%), and of the ligand-binding domain (58%). In contrast, the A/B domain, the hinge region and the F-domain are not conserved. Northern blot analysis revealed that ER beta is expressed in human thymus, spleen, ovary and testis. Transient transfections of an ER beta expression construct together with an ERE-based reporter construct in CHO cells clearly demonstrated transactivation of ER beta by 17 beta-estradiol. In addition, the ER alpha antagonist ICI-164384 is a potent antagonist for ER beta as well. Interestingly, the level of transactivation by 17 beta-estradiol is higher for ER alpha than for ER beta, which may reflect suboptimal conditions for ER beta at the level of the ligand, responsive element or cellular context.
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                Author and article information

                Journal
                Int J Mol Sci
                Int J Mol Sci
                ijms
                International Journal of Molecular Sciences
                MDPI
                1422-0067
                05 August 2017
                August 2017
                : 18
                : 8
                : 1713
                Affiliations
                [1 ]Ph.D. Program in Medical Biotechnology, College of Medical Science and Technology, Taipei Medical University, Taipei 110, Taiwan; lhhsu@ 123456kfsyscc.org
                [2 ]Division of Pulmonary and Critical Care Medicine, Sun Yat-Sen Cancer Center, Taipei 112, Taiwan
                [3 ]Department of Medicine, National Yang-Ming University Medical School, Taipei 112, Taiwan
                [4 ]Department of Medical Oncology, Sun Yat-Sen Cancer Center, Taipei 112, Taiwan; nmchu@ 123456kfsyscc.org
                [5 ]School of Medical Laboratory Science and Biotechnology, College of Medical Science and Technology, Taipei Medical University, Taipei 110, Taiwan
                Author notes
                [* ]Correspondence: kaosh@ 123456tmu.edu.tw ; Tel.: +886-2-2736-1661 (ext.3317); Fax: +886-2-2732-4510
                Author information
                https://orcid.org/0000-0003-4618-0898
                Article
                ijms-18-01713
                10.3390/ijms18081713
                5578103
                28783064
                bff39110-96ee-4942-95d3-faa85a1e82de
                © 2017 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 25 June 2017
                : 03 August 2017
                Categories
                Review

                Molecular biology
                epidermal growth factor receptor,estrogen,estrogen receptor,hormone,lung cancer,lung adenocarcinoma

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