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Differential expression of TGFbeta-stimulated clone 22 in normal prostate and prostate cancer
Cyrill A Rentsch1, Marco G Cecchini, Ruth Schwaninger
1Urology Research Laboratory, Departments of Urology and Clinical Research, University of Bern, Switzerland.
Abstract:
The transforming growth factor-beta (TGFbeta) 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 TGFbeta superfamily and functionally related genes between patient-matched noncancerous prostate (NP) and prostate cancer (PC) bulk tissue specimens highlighted two genes, namely TGFbeta-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.
Insights
Transforming growth factor-beta (TGFbeta) signaling is crucial for prostate health. This study identifies TSC-22 as a novel basal cell marker, showing its loss in prostate cancer indicates malignant transformation.
Area of Science:
- Molecular Biology
- Cancer Research
- Urology
Background:
- The transforming growth factor-beta (TGFbeta) superfamily regulates epithelial homeostasis.
- Altered TGFbeta signaling is implicated in prostate cancer development.
- Identifying key genes involved in prostate epithelial changes is crucial.
Purpose of the Study:
- To investigate differential gene expression of the TGFbeta superfamily in noncancerous prostate (NP) versus prostate cancer (PC).
- To identify novel molecular markers for prostate cancer diagnosis and study.
- To explore the role of TSC-22 in prostate carcinogenesis.
Main Methods:
- cDNA array analysis for differential gene expression.
- Real-time PCR for mRNA expression verification.
- Immunohistochemistry and immunoblotting for protein expression analysis.
Main Results:
- TGFbeta-stimulated clone-22 (TSC-22) was significantly underexpressed in PC tissues and cell lines compared to NP.
- Id4 gene expression did not show consistent alterations.
- TSC-22 protein was localized to basal cells in NP but absent in PC, suggesting it's a basal cell marker.
Conclusions:
- TSC-22 is a novel basal cell marker in the prostate epithelium.
- Loss of TSC-22 expression is associated with prostate malignant transformation.
- TSC-22 immunohistochemistry may serve as a diagnostic tool for distinguishing benign from malignant prostate lesions.
