scholarly journals Insulin-like growth factor 1 stimulation of androgen receptor activity requires β1A integrins

2011 ◽  
Vol 227 (2) ◽  
pp. 751-758 ◽  
Author(s):  
Aejaz Sayeed ◽  
Naved Alam ◽  
Marco Trerotola ◽  
Lucia R. Languino
Keyword(s):  
Androgen Receptor ◽  
Growth Factor ◽  
Receptor Activity ◽  
Insulin Like Growth Factor ◽  
Androgen Receptor Activity ◽  
Stimulation Of

scholarly journals НОВЫЕ ПАТОГЕНЕТИЧЕСКИЕ ФАКТОРЫ АНДРОГЕНЗАВИСИМЫХ ДЕРМАТОПАТИЙ

2019 ◽  
pp. 13-17
Author(s):  
Азимова Ф. В. ◽  
Ходжаева М. Б.
Keyword(s):  
Androgen Receptor ◽  
Growth Factor ◽  
Androgen Receptors ◽  
Receptor Activity ◽  
Insulin Like Growth Factor ◽  
Androgen Receptor Activity ◽  
Cytochrome P 450

This article is devoted to the study of coregulators of androgen receptor activity in the pathogenesis of androgen-dependent dermatopathies, in particular, for acne - 25-OH-VD, cytochrome p 450 (17-alpha hydroxylase), insulin-like growth factor. There were 46 patients with acne from 14 to 25 years of age under observation. The results of studies showed significant violations of the enzymes regulating androgen receptors - 25-OH-VD, cytochrome p 450 (17-alpha hydroxylase), as well as the growth factor (insulin-like growth factor), which are important in the pathogenesis of fast non-genomic molecular cell reactions of peripheral androgens metabolism with acne.

scholarly journals Interleukin-6 stimulation of growth of prostate cancer in vitro and in vivo through activation of the androgen receptor

2009 ◽  
Vol 16 (1) ◽  
pp. 155-169 ◽  
Author(s):  
Kamilla Malinowska ◽  
Hannes Neuwirt ◽  
Ilaria T Cavarretta ◽  
Jasmin Bektic ◽  
Hannes Steiner ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Interleukin 6 ◽  
Tumour Progression ◽  
Receptor Activity ◽  
Mitogen Activated Protein Kinase ◽  
Androgen Receptor Activity ◽  
Stimulation Of

It is hypothesized that ligand-independent activation of the androgen receptor is one of the mechanisms implicated in tumour progression. However, supportive evidence is limited to the effect of HER-2/neu that stimulates prostate cancer progression through activation of the androgen receptor. In the present study, we have asked whether the proinflammatory cytokine interleukin-6 (IL-6), which is known to stimulate androgen receptor activity and expression of its downstream target genes, may also induce growth of androgen-sensitive cells. We have found that IL-6 differentially regulates proliferation of LAPC-4 and MDA PCa 2b cells. In MDA PCa 2b cells, growth stimulation by IL-6 was reversed by administration of either the non-steroidal anti-androgen bicalutamide or the inhibitor of the mitogen-activated protein kinase pathway PD98059. Neither cell line was found to express endogenous IL-6. Interestingly, the treatment of those prostate cancer cells did not increase phosphorylation of STAT3. The effect of IL-6 on stimulation of androgen receptor activity in MDA PCa 2b cells was lower than that of androgen, comparable with findings reported by other researchers. However, growth of MDA PCa 2b xenografts in castrated animals treated with IL-6 was similar to that in non-castrated animals. In addition, bicalutamide showed an inhibitory effect on IL-6-regulated growth in vivo. Taken together, data in the present study demonstrate that IL-6 may cause growth of androgen receptor-positive tumours in vitro and in vivo through activation of the androgen receptor.

scholarly journals A novel DNA methylation signature is associated with androgen receptor activity and patient prognosis in bone metastatic prostate cancer

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Erik Bovinder Ylitalo ◽  
Elin Thysell ◽  
Mattias Landfors ◽  
Maria Brattsand ◽  
Emma Jernberg ◽  
...  
Keyword(s):  
Gene Expression ◽  
Prostate Cancer ◽  
Androgen Receptor ◽  
Bone Metastases ◽  
Metastatic Prostate Cancer ◽  
Tumor Biology ◽  
Receptor Activity ◽  
Mrna Levels ◽  
Androgen Receptor Activity ◽  
Patient Prognosis

Abstract Background Patients with metastatic prostate cancer (PC) are treated with androgen deprivation therapy (ADT) that initially reduces metastasis growth, but after some time lethal castration-resistant PC (CRPC) develops. A better understanding of the tumor biology in bone metastases is needed to guide further treatment developments. Subgroups of PC bone metastases based on transcriptome profiling have been previously identified by our research team, and specifically, heterogeneities related to androgen receptor (AR) activity have been described. Epigenetic alterations during PC progression remain elusive and this study aims to explore promoter gene methylation signatures in relation to gene expression and tumor AR activity. Materials and methods Genome-wide promoter-associated CpG methylation signatures of a total of 94 tumor samples, including paired non-malignant and malignant primary tumor areas originating from radical prostatectomy samples (n = 12), and bone metastasis samples of separate patients with hormone-naive (n = 14), short-term castrated (n = 4) or CRPC (n = 52) disease were analyzed using the Infinium Methylation EPIC arrays, along with gene expression analysis by Illumina Bead Chip arrays (n = 90). AR activity was defined from expression levels of genes associated with canonical AR activity. Results Integrated epigenome and transcriptome analysis identified pronounced hypermethylation in malignant compared to non-malignant areas of localized prostate tumors. Metastases showed an overall hypomethylation in relation to primary PC, including CpGs in the AR promoter accompanied with induction of AR mRNA levels. We identified a Methylation Classifier for Androgen receptor activity (MCA) signature, which separated metastases into two clusters (MCA positive/negative) related to tumor characteristics and patient prognosis. The MCA positive metastases showed low methylation levels of genes associated with canonical AR signaling and patients had a more favorable prognosis after ADT. In contrast, MCA negative patients had low AR activity associated with hypermethylation of AR-associated genes, and a worse prognosis after ADT. Conclusions A promoter methylation signature classifies PC bone metastases into two groups and predicts tumor AR activity and patient prognosis after ADT. The explanation for the methylation diversities observed during PC progression and their biological and clinical relevance need further exploration.

Anti-androgen receptor activity of apoptotic CK2 inhibitor CX4945 in human prostate cancer LNCap cells

2012 ◽  
Vol 22 (17) ◽  
pp. 5470-5474 ◽  
Author(s):  
Byung Jun Ryu ◽  
Seung-hwa Baek ◽  
Jiyeon Kim ◽  
Su Jung Bae ◽  
Sung-Youn Chang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Receptor Activity ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Lncap Cells ◽  
Androgen Receptor Activity ◽  
Ck2 Inhibitor

scholarly journals Stimulation of Mitochondrial Fatty Acid Oxidation by Growth Hormone in Human Fibroblasts1

1997 ◽  
Vol 82 (12) ◽  
pp. 4208-4213 ◽  
Author(s):  
Kin-Chuen Leung ◽  
Ken K. Y. Ho
Keyword(s):  
Fatty Acid ◽  
Growth Factor ◽  
Lipid Oxidation ◽  
Palmitic Acid ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Growth Factor I ◽  
Stimulation Of

In vivo administration of GH induces lipolysis and lipid oxidation. However, it is not clear whether the stimulation of lipid oxidation is a direct effect of GH or is driven by increased substrate supply secondary to lipolysis. An in vitro bioassay has been established for assessing β-oxidation of fatty acids in mitochondria, based on the measurement of conversion of tritiated palmitic acid to 3H2O by fibroblasts in culture. We have modified this assay to investigate whether GH stimulates fatty acid oxidation. GH stimulated oxidation of palmitic acid maximally by 26.7 ± 2.5% (mean ± sem; P < 0.0001). The stimulation was biphasic, with the oxidation rate increasing with increasing GH concentration to a peak response at 1.5 nmol/L and declining to a level not significantly different from control thereafter. Insulin-like growth factor-I at concentrations of up to 250 nmol/L had no significant effect on fatty acid oxidation. GH-binding protein attenuated the effect of GH. An anti-GH receptor (GHR) antibody (MAb263), which dimerizes the receptor and induces GH-like biological actions, significantly stimulated fatty acid oxidation. Another anti-GHR antibody (MAb5), which prevents receptor dimerization, suppressed GH action. In summary, GH directly stimulated fatty acid oxidation, an action not mediated by insulin-like growth factor-I. Dimerization of GHRs was necessary for this effect. This bioassay is a practical tool for studying the regulatory effects of GH on lipid oxidation.

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