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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

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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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Peder Rustøen Braadland and Alfonso Urbanucci

. 2010 ). Other TF motifs were also enriched in open chromatin regions of CRPC specimens, including glucocorticoid receptor (GR) motifs ( Urbanucci et al. 2017 ), which is in agreement with recent data showing its reactivation in CRPC ( Arora et al

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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.

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Sisi Liu, Emmanouil Saloustros, Annabel Berthon, Matthew F Starost, Isabelle Sahut-Barnola, Paraskevi Salpea, Eva Szarek, Fabio R Faucz, Antoine Martinez, and Constantine A Stratakis

to measure serum corticosterone levels in age-matched 9-month-old celecoxib-treated and control AdKO mice, as per the manufacturer's instructions. Studies of the glucocorticoid receptor in mouse adrenal glands RNA studies Frozen adrenals were

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Erin E Swinstead, Ville Paakinaho, and Gordon L Hager

needs to be further explored. For the SR family, the androgen receptor (AR) and the glucocorticoid receptor (GR) each have a multitude of functions in human biology and disease progression. In addition to ER and PR, AR and GR have also been implicated

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Yulia Koryakina, Karen E Knudsen, and Daniel Gioeli

studies on the glucocorticoid receptor (GR), progesterone receptor (PR), estrogen receptor (ER), and thyroid receptor (TR) have indicated that transcriptional activity is regulated as a function of the cell cycle ( Hsu & DeFranco 1995 , Maruvada et al