SOCS-3 Induces Myoblast Differentiation

Spangenburg, Espen E.

doi:10.1074/jbc.m410604200

Cited by 43 publications

(48 citation statements)

References 58 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…SOCS-3 is induced in response to IGF1 in neurons, and antagonises its effect on survival through binding to the IGFR1 (Yadav et al 2005). IGF1 also upregulates SOCS-3 during differentiation of myoblasts, thus inducing transcriptional activation of the a-actin promoter (Spangenburg 2005).…”

Section: Socs-3 Is a Regulator Of Receptor Tyrosine Kinasesmentioning

confidence: 99%

SOCS-3 antagonises the proliferative and migratory effects of fibroblast growth factor-2 in prostate cancer by inhibition of p44/p42 MAPK signalling

Puhr¹,

Santer²,

Neuwirt³

et al. 2010

Endocrine-Related Cancer

View full text Add to dashboard Cite

Fibroblast growth factor-2 (FGF-2) is highly expressed in prostate cancer. It promotes tumour progression through multiple pathways including those of signal transducers and activators of transcription factor 3 (STAT3), mitogen-activated protein kinases (MAPKs) and Akt. In previous studies, we have reported that STAT3 phosphorylation inversely correlates with suppressor of cytokine signalling-3 (SOCS-3) expression in prostate cancer cells. Recently, it has become evident that SOCS-3-negative regulation is not only limited to the interleukin-6 (IL-6) receptor. We hypothesised that SOCS-3 interferes with FGF signalling, thus influencing the outcome of its action in prostate cancer cells. For this purpose, we treated DU-145 and LNCaP-IL-6C cells with increasing concentrations of FGF-2, and verified protein phosphorylation. In the presence of FGF-2, neither STAT3, STAT1, nor Akt could be phosphorylated. Solely the p44/p42 MAPK pathway was activated after FGF-2 stimulation. We show for the first time that SOCS-3 interferes with the FGF-2 signalling pathway by modulating p44 and p42 phosphorylation in prostate cancer cells. Decreased SOCS-3 protein expression results in increased MAPK phosphorylation, whereas SOCS-3 overexpression leads to a decreased cellular proliferation and migration. On the basis of the present results, we propose that SOCS-3 is a novel modulator of FGF-2-regulated cellular events in prostate cancer.

show abstract

Section: Socs-3 Is a Regulator Of Receptor Tyrosine Kinasesmentioning

confidence: 99%

SOCS-3 antagonises the proliferative and migratory effects of fibroblast growth factor-2 in prostate cancer by inhibition of p44/p42 MAPK signalling

Puhr¹,

Santer²,

Neuwirt³

et al. 2010

Endocrine-Related Cancer

View full text Add to dashboard Cite

show abstract

“…It was recognized several years ago that SOCS2 could interact with and inhibit the IGF-1R [52]. It has been subsequently demonstrated that not only could IGF-1R be affected by SOCS proteins, but that IGF-1R signaling could upregulate the expression of SOCS3 directly [53]. Stem cell factor (SCF) receptor (kit) is another receptor tyrosine kinase that is relevant to hematopoietic recovery since it is expressed on a variety of stem cells.…”

Section: Socs Effects On Receptor Tyrosine Kinasesmentioning

confidence: 99%

Neuroendocrine hormones such as growth hormone and prolactin are integral members of the immunological cytokine network

Redelman¹,

Taub

et al. 2008

Cellular Immunology

View full text Add to dashboard Cite

Neuroendocrine hormones such as growth hormone (GH) and prolactin (PRL) have been demonstrated to accelerate the recovery of the immune response after chemotherapy and bone marrow transplantation and to enhance the restoration of immunity in individuals infected with HIV and in normal individuals with compromised immune systems associated with aging. As the mechanism of action of these hormones has been elucidated, it has become clear that they are integral members of the immunological cytokine/chemokine network and share regulatory mechanisms with a wide variety of cytokines and chemokines. The members of this cytokine network induce and can be regulated by members of the suppressor of cytokine signaling (SOCS) family of intracellular proteins. In order to take advantage of the potential beneficial effects of hormones such as GH or PRL, it is essential to take into consideration the overall cytokine network and the regulatory effects of SOCS proteins.

show abstract

“…Furthermore, SOCS-3 has been identified as a regulator of myoblast differentiation. 18 To understand better the mechanisms of IL-6/JAK/ STAT3 signaling in benign and malignant prostate tissue, we have assessed expression of SOCS-3 in prostate cells and in material obtained from patients. The mechanisms responsible for changes in SOCS-3 expression were investigated.…”

mentioning

confidence: 99%

Suppressor of Cytokine Signaling-3 Antagonizes cAMP Effects on Proliferation and Apoptosis and Is Expressed in Human Prostate Cancer

Bellezza

Neuwirt

Nemes

et al. 2006

The American Journal of Pathology

View full text Add to dashboard Cite

Interleukin-6, levels of which are elevated in prostate cancer, activates different signal transduction pathways including that of Janus kinases/signal transducer and activator of transcription (STAT)3. However, phosphorylation of STAT3 has been reported to be associated with either stimulatory or inhibitory effects on cellular proliferation. To better understand the mechanisms of STAT3 regulation in benign and malignant prostate, we have investigated the role of suppressor of cytokine signaling (SOCS)-3. Cell lines that did not express phosphorylated STAT3 were found to be SOCS-3-positive. SOCS-3 was re-expressed in LNCaP cells after treatment with a demethylating agent. SOCS-3 immunohistochemistry revealed a negative or weak reaction in benign areas , whereas its expression was detected in tumor tissue. To investigate the involvement of SOCS-3 in regulation of cellular events , we incubated cancer cells with a cAMP derivative. This treatment yielded higher SOCS-3 levels , reduced [ 3 H]thymidine incorporation , and increased percentage of apoptotic cells. However , down-regulation of SOCS-3 by a short interfering RNA approach resulted in inhibition of proliferation and an increased apoptotic rate. Collectively , our results show that SOCS-3 antagonizes regulation of cellular events by cAMP and is expressed in human prostate cancer.

show abstract

SOCS-3 Induces Myoblast Differentiation

Cited by 43 publications

References 58 publications

SOCS-3 antagonises the proliferative and migratory effects of fibroblast growth factor-2 in prostate cancer by inhibition of p44/p42 MAPK signalling

SOCS-3 antagonises the proliferative and migratory effects of fibroblast growth factor-2 in prostate cancer by inhibition of p44/p42 MAPK signalling

Neuroendocrine hormones such as growth hormone and prolactin are integral members of the immunological cytokine network

Suppressor of Cytokine Signaling-3 Antagonizes cAMP Effects on Proliferation and Apoptosis and Is Expressed in Human Prostate Cancer

Contact Info

Product

Resources

About