Cancer Cell Biology
Differential expression of TGFβ-stimulated clone 22 in normal prostate and prostate cancer†
Article first published online: 16 AUG 2005
Copyright © 2005 Wiley-Liss, Inc.
International Journal of Cancer
Volume 118, Issue 4, pages 899–906, 15 February 2006
How to Cite
Rentsch, C. A., Cecchini, M. G., Schwaninger, R., Germann, M., Markwalder, R., Heller, M., van der Pluijm, G., Thalmann, G. N. and Wetterwald, A. (2006), Differential expression of TGFβ-stimulated clone 22 in normal prostate and prostate cancer. Int. J. Cancer, 118: 899–906. doi: 10.1002/ijc.21449
The authors declare no conflict of interest related to the matter disclosed in this manuscript.
- Issue published online: 13 DEC 2005
- Article first published online: 16 AUG 2005
- Manuscript Accepted: 27 JUN 2005
- Manuscript Received: 31 MAR 2005
- Swiss National Foundation. Grant Number: 3200-068409.02
- Bernische Krebsliga (From the Benchside to Bedside – Prevention, Detection and Treatment of Micrometastases)
- The Genera Foundation
- European Commission Grant. Grant Number: PRIMA-504587
- prostate cancer;
- TGFβ superfamily;
- basal cell marker
The transforming growth factor-β (TGFβ) superfamily and its downstream effector genes are key regulators of epithelial homeostasis. Altered expression of these genes may be associated with malignant transformation of the prostate gland. The cDNA array analysis of differential expression of the TGFβ superfamily and functionally related genes between patient-matched noncancerous prostate (NP) and prostate cancer (PC) bulk tissue specimens highlighted two genes, namely TGFβ-stimulated clone-22 (TSC-22) and Id4. Verification of their mRNA expression by real-time PCR in patient-matched NP and PC bulk tissue, in laser-captured pure epithelial and cancer cells and in NP and PC cell lines confirmed TSC-22 underexpression, but not Id4 overexpression, in PC and in human PC cell lines. Immunohistochemical analysis showed that TSC-22 protein expression in NP is restricted to the basal cells and colocalizes with the basal cell marker cytokeratin 5. In contrast, all matched PC samples lack TSC-22 immunoreactivity. Likewise, PC cell lines do not show detectable TSC-22 protein expression as shown by immunoblotting. TSC-22 should be considered as a novel basal cell marker, potentially useful for studying lineage determination within the epithelial compartment of the prostate. Conversely, lack of TSC-22 seems to be a hallmark of malignant transformation of the prostate epithelium. Accordingly, TSC-22 immunohistochemistry may prove to be a diagnostic tool for discriminating benign lesions from malignant ones of the prostate. The suggested tumour suppressor function of TSC-22 warrants further investigation on its role in prostate carcinogenesis and on the TSC-22 pathway as a candidate therapeutic target in PC. © 2005 Wiley-Liss, Inc.