Cancer-Specific Loss of Urocortin 3 in Human Renal Cancer
Introduction The corticotropin-releasing hormone (CRH) system, its receptors corticotropin-releasing hormone receptor 1 (CRHR1) and 2 (CRHR2), and its corresponding binding protein corticotropin-releasing hormone-binding protein (CRHBP) as well as the urocortin proteins—structural homologues to CRH,...
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Veröffentlicht in: | Advances in therapy 2020, Vol.37 (1), p.288-299 |
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Sprache: | eng |
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Zusammenfassung: | Introduction
The corticotropin-releasing hormone (CRH) system, its receptors corticotropin-releasing hormone receptor 1 (CRHR1) and 2 (CRHR2), and its corresponding binding protein corticotropin-releasing hormone-binding protein (CRHBP) as well as the urocortin proteins—structural homologues to CRH, which are included in this peptide family—have become interesting oncological targets recently. Carcinogenesis of various human tumors has been reported with an altered presence of members of this system. The aim of the present study was to examine the role of urocortin 3 (UCN3) in renal cell carcinoma (RCC).
Methods
Therefore, tumoral tissues of 106 patients with RCC and available corresponding normal tissues were analyzed using qPCR for quantitative mRNA expression analysis. Tissue localization and protein signals of UCN3 in normal and tumoral renal specimens were evaluated using western blot and immunohistochemistry. In addition, correlation studies of
UCN3
mRNA expression with clinicopathological parameters of patients with RCC and different histological subtypes were evaluated.
Results
UCN3
mRNA was significantly downregulated in nearly all tumoral tissues (
p
= 7.92 × 10
−13
). The same effect was observed at protein level using immunohistochemistry. Level of
UCN3
mRNA expression was not directly correlated with clinicopathological parameters.
Conclusion
We report for the first time the significant downregulation of UCN3 in RCC. These results demonstrate a possible involvement of the CRH system and its significance in carcinogenesis of RCC. |
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ISSN: | 0741-238X 1865-8652 |
DOI: | 10.1007/s12325-019-01141-y |