Artikel
The involvement of Wnt/beta-catenin pathway in pituitary adenomas
Der Einfluss des Wnt/beta-catenin-Weges auf Hypophysenadenome
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Veröffentlicht: | 11. April 2007 |
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Gliederung
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Objective: The pituitary neoplasm is the third most common tumour developing in the human cranial cavity. Altered Wnt/beta-catenin signalling has recently been recognized to be associated with the development of various human cancers. Wnt stabilizes beta-catenin (free beta-catenin) by preventing its normal phosphorylation which targets beta-catenin for degradation. Free beta-catenin is translocated to the nucleus where it stimulates a number of genes involved in proliferation and differentiation control upon binding to TCF/LEF-1. The aim of the present study was to investigate the role of the Wnt/beta-catenin pathway in a series of pituitary adenomas.
Methods: Samples of 10 growth hormone secreting, 10 hormone inactive adenomas and 4 normal adenohypophyseal glands were studied by Western blot analyses, direct DNA sequencing, single strand conformation polymorphism and RT-PCR.
Results: The beta-catenin expression was high at protein and RNA levels in both GH secreting and hormone inactive pituitary adenomas as compared to normal pituitary tissues. The expression of cyclin D1, a target gene of Wnt/beta-catenin signalling, was found only in GH-secreting and hormone inactive adenomas, but was undetectable in the normal pituitary. Specific mutations in exon 3 of CTNNB1 are rare in the pituitary adenomas according to our study.
Conclusions: We suggest that there is an involvement of the Wnt/beta-catenin pathway in pituitary adenomas, but not through beta-catenin exon 3 mutations. The overexpression of beta-catenin and cyclin D1 underlines the potential importance of beta-catenin deregulation for the pathophysiology of pituitary adenomas.