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Jan Kroon, Martin Puhr, Jeroen T Buijs, Geertje van der Horst, Daniëlle M Hemmer, Koen A Marijt, Ming S Hwang, Motasim Masood, Stefan Grimm, Gert Storm, Josbert M Metselaar, Onno C Meijer, Zoran Culig, and Gabri van der Pluijm

underlying molecular mechanisms of docetaxel resistance is of a pivotal importance to combat docetaxel resistance in clinics ( Madan et al . 2011 ). The glucocorticoid receptor (GR) is a receptor that, upon binding of glucocorticoids (GCs) (e

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G Schlossmacher, E Platt, A Davies, S Meredith, and A White

investigation of the glucocorticoid receptor (GR) expression in SCLC cell lines. A multitude of factors can affect Gc sensitivity and we have previously shown that some human SCLC cell lines are resistant to Gcs and that this resistance is due to impaired GR

Open access

Paula Sommer, Rachel L Cowen, Andrew Berry, Ann Cookson, Brian A Telfer, Kaye J Williams, Ian J Stratford, Paul Kay, Anne White, and David W Ray

immunosuppression. Their action is mediated by the glucocorticoid receptor (GR) which belongs to the nuclear receptor superfamily. The inability of Gcs to inhibit ACTH precursor expression in SCLCs prompted investigation of GR expression in SCLCs. We ( Ray et al

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Alba Jiménez-Panizo, Paloma Pérez, Ana M Rojas, Pablo Fuentes-Prior, and Eva Estébanez-Perpiñá

), the glucocorticoid receptor (GR/NR3C1), the mineralocorticoid receptor (MR/NR3C2) and the progesterone receptor (PR/NR3C3). Phylogenetic studies show that AR, GR, MR and PR comprise a subfamily of so-called oxosteroid NRs, which markedly differ from

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Paolo Vigneri, Francesco Frasca, Laura Sciacca, Giuseppe Pandini, and Riccardo Vigneri

insulin levels increase (as in the post-prandial surge in insulin-resistant subjects or after insulin injection), insulin may bind and activate the related insulin-like growth factor-I (IGF-I) receptor, which shares ∼80% homology with the insulin receptor

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Yuanzhong Wang, Yen-Dun Tony Tzeng, Gregory Chang, Xiaoqiang Wang, and Shiuan Chen

Introduction Approximately 70% breast cancers are estrogen receptor positive (ER+), and endocrine therapy is the main treatment for ER+ breast cancer patients. Selective ER modulators (e.g. tamoxifen) and aromatase inhibitors (AIs) constitute

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Yu-Xia Chen, Yan Wang, Chen-Chun Fu, Fei Diao, Liang-Nian Song, Zong-Bin Li, Rui Yang, and Jian Lu

chemotherapy . Blood 83 65 – 71 . Li Z Chen Y Cao D Wang Y Chen G Zhang S Lu J 2006 Glucocorticoid up-regulates transforming growth factor-beta (TGF-beta) type II receptor and enhances TGF

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V Craig Jordan

.003). Figure 5 Steroids with the ability to bind to the progesterone receptor, estrogen receptor, glucocorticoid receptor, or multiple receptors. In the Million Women's study ( Beral et al . 2003 ), 1 129 025 postmenopausal women were recruited

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Isabel Mayayo-Peralta, Wilbert Zwart, and Stefan Prekovic

Glucocorticoid receptor (GR) is a key homeostatic regulator involved in governing immune response, neuro-integration, metabolism and lung function. In conjunction with its pivotal role in human biology, GR action is critically linked to pathology of various disease types, including cancer. While pharmacological activation of GR has been used for treatment of various liquid cancers, its role in solid cancers is less clearly defined and seems to be cancer-type dependent. This review focuses on the molecular aspects of GR biology, spanning the structural and functional basis of response to glucocorticoids, as well as how this transcription factor operates in cancer, including the implications in disease development, progression and drug resistance.

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W-D Han, Y-M Mu, X-C Lu, Z-M Xu, X-J Li, L Yu, H-J Song, M Li, J-M Lu, Y-L Zhao, and C-Y Pan

LRP16 is a novel gene cloned from lymphocytic cells, and its function is not known. The expression level of LRP16 mRNA was up-regulated by estrogen in breast cancer MCF-7 cells based on the computed aided serial analysis of gene expression (SAGE) analysis. In this study, we investigate the effect of 17beta-estradiol (17beta-E(2)) on the expression of LRP16 mRNA and the effects of overexpression of LRP16 on the proliferation of cultured MCF-7 cells and the possible mechanisms involved. The expression level of LRP16 mRNA induced by 17beta-E(2) was determined by Northern blot analysis. LRP16 promoter-controlled luciferase expression vector (pGL3-S(0)) was co-transfected with various nuclear receptors, including estrogen receptor alpha and beta (ERalpha and ERbeta), glucocorticoid receptor alpha (GRalpha), androgen receptor (AR) and peroxisome-proliferator activated receptor gamma and alpha (PPARgamma and PPARgamma) into COS-7 cells, and the relative luciferase activity was measured using Dual-luciferase report assay systems. The effect of overexpression of LRP16 on MCF-7 proliferation was examined by the Trypan Blue exclusion method, and the cell cycle was analyzed by flow cytometry. The expression levels of cyclin E, p53 and p21(WAF1/CIP1) proteins were determined by Western blot analysis. The results showed (1) 17beta-E(2) induced a five- to eightfold increase in LRP16 mRNA levels in MCF-7 cells; (2) the relative luciferase activities in the COS-7 cells co-transfected by pGL3-S(0) and ERalpha or AR were 7.8-fold and 11-fold respectively of those in the control cells transfected by pGL3-S(0) alone; (3) overexpression of LRP16 stimulated MCF-7 cell proliferation, and the numbers of cells in the S-phase of the cell cycle in cells transfected with LRP16 increased about 10% compared with the control cells; and (4) cyclin E levels were much higher in cells with overexpression of LRP16 than in the control cells, while the expression levels of p53 and p21(WAF1/CIP1) were not different between the two groups of cells. From these results we concluded that estrogen up-regulates the expression level of LRP16 mRNA through activation of ERalpha and that overexpression of LRP16 promotes MCF-7 cell proliferation probably by increasing cyclin E.