TITLE

Growth/differentiation factor-15: prostate cancer suppressor or promoter?

AUTHOR(S)
Vaňhara, P; Hampl, A; Kozubík, A; Souček, K
PUB. DATE
December 2012
SOURCE
Prostate Cancer & Prostatic Diseases;2012, Vol. 15 Issue 4, p320
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Deregulation of expression and function of cytokines belonging to the transforming growth factor-β (TGF-β) family is often associated with various pathologies. For example, this cytokine family has been considered a promising target for cancer therapy. However, the detailed functions of several cytokines from the TGF-β family that could have a role in cancer progression and therapy remain unclear. One of these molecules is growth/differentiation factor-15 (GDF-15), a divergent member of the TGF-β family. This stress-induced cytokine has been proposed to possess immunomodulatory functions and its high expression is often associated with cancer progression, including prostate cancer (PCa). However, studies clearly demonstrating the mechanisms for signal transduction and functions in cell interaction, cancer progression and therapy are still lacking. New GDF-15 roles have recently been identified for modulating osteoclast differentiation and for therapy for PCa bone metastases. Moreover, GDF-15 is as an abundant cytokine in seminal plasma with immunosuppressive properties. We discuss studies that focus on the regulation of GDF-15 expression and its role in tissue homeostasis, repair and the immune response with an emphasis on the role in PCa development.
ACCESSION #
83355974

 

Related Articles

  • Understanding stress-induced immunosuppression: Exploration of cytokine and chemokine gene profiles in chicken peripheral leukocytes. Shini, S.; Huff, G. R.; Shini, A.; Kaiser, P. // Poultry Science;Apr2010, Vol. 89 Issue 4, p841 

    At present, the poultry meat and egg industry has gained a lot of ground, being viewed as a provider of a healthy alternative to red meat and other protein sources. If this trend is to be maintained, solutions must be found to improve resistance of chickens to disease, which often is weakened by...

  • Kinases: Making gains on glioma. Owens, Joanna // Nature Reviews Drug Discovery;Dec2004, Vol. 3 Issue 12, p999 

    Reports on a paper published in the journal "Cancer Research" indicating that a small-molecule inhibitor of transforming growth factor-Î’ (TGF-Î’) receptor I kinase could prove to be an effective treatment for human gliomas. Effect of the investigational drug SD-208 on the...

  • TGF-β upregulates CD70 expression and induces exhaustion of effector memory T cells in B-cell non-Hodgkin's lymphoma. Yang, Z-Z; Grote, D M; Xiu, B; Ziesmer, S C; Price-Troska, T L; Hodge, L S; Yates, D M; Novak, A J; Ansell, S M // Leukemia (08876924);Sep2014, Vol. 28 Issue 9, p1872 

    Transforming growth factor beta (TGF-β) has an important role in mediating T-cell suppression in B-cell non-Hodgkin lymphoma (NHL). However, the underlying mechanism responsible for TGF-β-mediated inhibition of effector memory T (Tm) cells is largely unknown. As reported here, we show that...

  • The impact of perinatal immune development on mucosal homeostasis and chronic inflammation. Renz, Harald; Brandtzaeg, Per; Hornef, Mathias // Nature Reviews Immunology;Jan2012, Vol. 12 Issue 1, p9 

    The mucosal surfaces of the gut and airways have important barrier functions and regulate the induction of immunological tolerance. The rapidly increasing incidence of chronic inflammatory disorders of these surfaces, such as inflammatory bowel disease and asthma, indicates that the immune...

  • New Drugs in Oncology/New Diagnosis and Modalities in Cancer Therapy.  // Journal of Cancer Research & Clinical Oncology;2004 Supplement 1, Vol. 130, pS148 

    Presents abstracts of articles about new drugs on oncology and new diagnosis and modalities in cancer therapy. Preclinical efficacy data of transforming growth-factor- beta 2 suppression in pancreatic cancer by the antisense oligonucleotide AP 12009; Lipoptosis, tumor cell death by...

  • Inhibition of TGF-β signaling with halofuginone can enhance the antitumor effect of irradiation in Lewis lung cancer. Runlong Lin; Shuai Yi; Linlin Gong; Weishuai Liu; Peng Wang; Ningbo Liu; Lujun Zhao; Ping Wang // OncoTargets & Therapy;Dec2015, Vol. 8, p3549 

    Purpose: It was reported that halofuginone has inhibitory effects on transforming growth factor-beta (TGF-β) signaling pathway. The study was aimed to: 1) evaluate the antitumor effects of halofuginone in combination with radiation therapy; and 2) preliminarily explore the possible mechanisms...

  • The underlying cellular mechanism of fibrosis. RODEMANN, H. PETER; BINDER, ANKE; BURGER, ANKE; GÜVEN, NURI; LÖFFLER, HEIDI; BAMBERG, MICHAEL // Kidney International Supplement;May1996, Issue 54, pS-32 

    Fibrosis is a common sequela of various exogenous insults to a variety of parenchymal tissues. The underlying mechanisms of the induction and progression of fibrosis both at the molecular and cellular level have not been clarified so far. In the present study the cellular level have not been...

  • Transdifferentiation of hepatic stellate cells (Ito cells) to myofibroblasts: A key event in hepatic fibrogenesis. GRESSNER, A. M. // Kidney International Supplement;May1996, Issue 54, pS-39 

    Hepatic stellate cells (HSC) are the major source of extracellular matrix components (ECM), if these precursor cells are activated in areas of necroinflammation to proliferate and to transdifferentiate from the retinoid storing to the ECM-producing phenotype termed myofibroblast (MFB). the...

  • Role of the myofibroblast in pulmonary fibrosis. PHAN, SEM H. // Kidney International Supplement;May1996, Issue 54, pS-46 

    The authors discuss the origination of myofibroblasts with alpha-smooth muscle actin phenotype that are found in pulmonary fibrosis. They mention that the myofibroblasts could be influenced by cytokines such as transforming growth factors-beta. Myofibroblasts may be the primary cause of...

Share

Read the Article

Courtesy of THE LIBRARY OF VIRGINIA

Sorry, but this item is not currently available from your library.

Try another library?
Sign out of this library

Other Topics