More than an accessory: implications of type III transforming growth factor‐β receptor loss in prostate cancer

Ajiboye, Seun; Sissung, Tristan M.; Sharifi, Nima; Figg, William D.

doi:10.1111/j.1464-410x.2009.08999.x

Cited by 15 publications

(12 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Rapamycin (78) and soy isoflavones (79), plant-derived polyphenolic compounds with estrogen-like properties, inhibit prostate cancer cell growth and are associated with a decrease in the expression of FST. Type III TGFβ receptor has been reported to play an inhibitory role in the growth of prostate cancer cells (80). FST has been shown to directly bind to and completely block type III TGFβ receptor-induced epithelialmesenchymal transition of normal murine mammary gland epithelial cell line in vitro (60) and thus might promote prostate cell proliferation by targeting this receptor.…”

Section: Follistatin In the Development And Progression Of Solid Tumoursmentioning

confidence: 99%

Clinical and Therapeutic Implications of Follistatin in Solid Tumours

Shi

Resaul

Owen

et al. 2016

CGP

View full text Add to dashboard Cite

Abstract. Follistatin (FST) Follistatin (FST), which was first isolated from porcine and bovine follicular fluid (1, 2), was initially described as a protein involved in the regulation of the secretion of folliclestimulating hormone. This monomeric glycosylated polypeptide chain is encoded by a single gene located on the long arm chromosome 5q11.2 (3), which through alternative splicing may be transcribed into the mRNA precursors, FST317 and FST344. From these precursors, three major FST isoforms may be produced, namely FST288 (from pre-FST317), FST315 (from pre-FST344) and a third FST isoform, FST303, produced from the post-translational truncation of the FST315 C-terminus. These three main FST isoforms can also be glycosylated to yield six further FST isoforms that were previously identified in bovine (4) and porcine (5, 6) follicular fluid. At the core, all FST isoforms contain a 63 residue N-terminal domain and three follistatin domains, termed FSD1, FSD2 and FSD3. These domains comprise 73-77 amino acid residues and are characterised by an arrangement of 10 conserved cysteine residues (7). Both FST288 and FST315 are differentially expressed in human tissues (6-9). FST315 is the predominant isoform, whilst the FST288 isoform accounts for less than 5% of the encoded mRNA (10, 11). Some molecules such as activin, transforming growth factor-beta (TGFβ), forkhead domain transcription factor L2 (12, 13), gonadotropin-releasing hormone (14), zinc finger protein (GLI2) (15), dexamethasone (16), androgens (17), activators of winglessrelated integration site (WNT) signalling (18, 19) and 1,25-dihydroxyvitamin D (20) have been shown to regulate the transcription of the FST gene. In addition, down-regulation of FST gene expression by peroxisome proliferator-activated receptor gamma (PPARγ) or the transcription factor epiprofin (21, 22) has been shown.As an antagonist of TGFβ superfamily member activin, FST seems to primarily function in relation to the role that activin plays. Along with FST, activin acts as a pleiotropic growth factor system, which is involved in proliferation, differentiation, and apoptosis of a number of cell types (23-28). As such, the functions of the FST isoforms are therefore linked to their binding affinity for activin (6,10,11,(29)(30)(31)(32)(33)(34)(35)(36)(37). In fact, this critical binding and neutralisation of activin, either partial or complete, is based on the order of at least two of the FST cysteine domains and its Nterminal (38), conferring a difference in affinities for activin between the FST isoforms. The binding complex between activin and FST generally occurs in a 1:2 ratio, where the two FST molecules, connected C-terminus to N-425

show abstract

Section: Follistatin In the Development And Progression Of Solid Tumoursmentioning

confidence: 99%

Clinical and Therapeutic Implications of Follistatin in Solid Tumours

Shi

Resaul

Owen

et al. 2016

CGP

View full text Add to dashboard Cite

show abstract

“…ActR-II and IIB bind to activins when expressed alone or jointly with activin type I receptors, or bind to BMPs 2, 4 and 7 and GDF5 in concert with BMPR-I (Buijs et al 2007). In addition to these two major types of receptors, type III TGF-β receptor (TβRIII) or betaglycan is reported as an accessory receptor (Ajiboye et al 2010). This TβRIII is ubiquitously expressed but does not have an intrinsic signaling function.…”

Section: Tgf-β Signalingmentioning

confidence: 99%

“…This TβRIII is ubiquitously expressed but does not have an intrinsic signaling function. TβRIII participates in the regulation of TGF-β signaling and has recently been identified as a tumor suppressor (Ajiboye et al 2010;You et al 2009). …”

Section: Tgf-β Signalingmentioning

confidence: 99%

Transforming growth factor-β signaling in tumor initiation, progression and therapy in breast cancer: an update

Zhang

Cao

et al. 2011

Cell Tissue Res

View full text Add to dashboard Cite

Transforming growth factor-β (TGF-β) is a ubiquitous cytokine playing an essential role in cell proliferation, differentiation, apoptosis, adhesion and invasion, as well as in cellular microenvironment. In malignant diseases, TGF-β signaling features a growth inhibitory effect at an early stage but aggressive oncogenic activity at the advanced malignant state. Here, we update the current understanding of TGF-β signaling in cancer development and progression with a focus on breast cancer. We also review the current approaches of TGF-β signaling-targeted therapeutics for human malignancies.

show abstract

“…NKX3.1 has an indispensable role in prostate cancer and is regarded as the “gatekeeper” to prevent tumorigenesis[50,52]. Subsequent GWAS using Tobagonian men as the replication sample have not found an association between prostate tumor development and TGFBR3, a tumor suppressor with a significant role in prostate tumor development [53,54]. These data suggest that the mechanism which produces tumorigenesis in prostate cells or other cell types could have different associated genetic variants in some non-European populations.…”

Section: Notable Discoveries From Gwas In African American and Africamentioning

confidence: 99%

Genome-Wide Association Studies in Africans and African Americans: Expanding the Framework of the Genomics of Human Traits and Disease

Peprah

Tekola‐Ayele

et al. 2014

Public Health Genomics

View full text Add to dashboard Cite

Genomic research is one of the tools for elucidating the pathogenesis of diseases of global health relevance and paving the research dimension to clinical and public health translation. Recent advances in genomic research and technologies have increased our understanding of human diseases, genes associated with these disorders, and the relevant mechanisms. Genome-wide association studies (GWAS) have proliferated since the first studies were published several years ago and have become an important tool in helping researchers comprehend human variation and the role genetic variants play in disease. However, the need to expand the diversity of populations in GWAS has become increasingly apparent as new knowledge is gained about genetic variation. Inclusion of diverse populations in genomic studies is critical to a more complete understanding of human variation and elucidation of the underpinnings of complex diseases. In this review, we summarize the available data on GWAS in recent African ancestry populations within the western hemisphere (i.e. African Americans and peoples of the Caribbean) and continental African populations. Furthermore, we highlight ways in which genomic studies in populations of recent African ancestry have led to advances in the areas of malaria, HIV, prostate cancer, and other diseases. Finally, we discuss the advantages of conducting GWAS in recent African ancestry populations in the context of addressing existing and emerging global health conditions.

show abstract

More than an accessory: implications of type III transforming growth factor‐β receptor loss in prostate cancer

Cited by 15 publications

References 22 publications

Clinical and Therapeutic Implications of Follistatin in Solid Tumours

Clinical and Therapeutic Implications of Follistatin in Solid Tumours

Transforming growth factor-β signaling in tumor initiation, progression and therapy in breast cancer: an update

Genome-Wide Association Studies in Africans and African Americans: Expanding the Framework of the Genomics of Human Traits and Disease

Contact Info

Product

Resources

About