Abstract:
:Inhibin is a member of the TGF-beta superfamily of growth and differentiation factors and a tumor suppressor. Consistent with the tumor suppressive function of the inhibin alpha subunit in prostate cancer, we reported a loss of gene expression due to DNA hypermethylation and loss of heterozygosity (LOH) as well as down regulation of inhibin alpha subunit immunoreactivity. Paradoxically, an expanded study to evaluate the prognostic significance of inhibin alpha subunit expression in men with prostate cancer resulted in a contradictory outcome, whereby an up-regulation of subunit expression was recorded. In seeking a more comprehensive explanation for all data sets, we offer a unifying hypothesis. We propose that the tumor suppressor activities of the inhibin alpha subunit dominate in non-malignant tissue, but its oncogenic activities emerge during tumorigenesis. An explanation such as this, involving a switch in gene function from being tumor suppressive to pro-oncogenic, may account for the discrepant findings in other types of cancer.
journal_name
Mol Cell Endocrinoljournal_title
Molecular and cellular endocrinologyauthors
Risbridger GP,Ball EM,Wang H,Mellor SL,Peehl DMdoi
10.1016/j.mce.2004.02.015keywords:
subject
Has Abstractpub_date
2004-10-15 00:00:00pages
73-6issue
1-2eissn
0303-7207issn
1872-8057pii
S0303720704000772journal_volume
225pub_type
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