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Molecular analysis of the INK4 family of genes in prostate carcinomas
D J Park1, S P Wilczynski, E Y Pham
1Division of Hematology/Oncology, Cedars-Sinai Medical Center, UCLA School of Medicine, Los Angeles, California 90048, USA.
Purpose:
A newly recognized class of INK4 family of cyclin-dependent kinase inhibitors CDKIs) include its prototype, p16 (INK4A/MTS1/CDKN2), and three others, p15 (INK4B/MTS2), p18 (INK4C), and p19 (INK4D). The putative tumor suppressor gene, p16 is frequently altered in certain neoplasms and many cell lines. The potential role of INK4 CDKIs in pathogenesis of prostate carcinoma was studied.
Materials And Methods:
Thirty-two primary prostate cancer samples and two prostate cancer cell lines were examined for alterations of the p16, p15, p18, and p19 genes by polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) and Southern blot analysis.
Results:
Alteration of the p16 gene was found in one of 32 primary prostate cancer samples by PCR-SSCP. DNA sequencing of the sample showed a 24-basepair insertion in exon 1 of the p16 gene at codon 11. No other mutations were found in p15, p18, or p19 genes by PCR-SSCP. Furthermore, none of the p16, p15, p18, or p19 genes had alterations by Southern blot analysis.
Conclusions:
These results indicate that structural abnormalities of the INK4 CDKIs is a rare event in prostate carcinoma, and the loss of function of INK4 CDKIs by other mechanisms, such as methylation should be further explored.
Insights
Structural abnormalities in INK4 cyclin-dependent kinase inhibitors (CDKIs) are rare in prostate cancer. Further research into other mechanisms, like methylation, is needed to understand their role in prostate carcinoma development.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- The INK4 family of cyclin-dependent kinase inhibitors (CDKIs) includes p16, p15, p18, and p19.
- The p16 gene is a known tumor suppressor frequently altered in various cancers.
- The role of INK4 CDKIs in prostate carcinoma pathogenesis requires investigation.
Purpose of the Study:
- To investigate the potential role of INK4 CDKIs in the pathogenesis of prostate carcinoma.
- To examine alterations in the p16, p15, p18, and p19 genes in prostate cancer samples.
Main Methods:
- Analysis of 32 primary prostate cancer samples and two cell lines.
- Utilized polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) and Southern blot analysis.
- Examined structural alterations in p16, p15, p18, and p19 genes.
Main Results:
- A single alteration (24-basepair insertion in exon 1) was detected in the p16 gene in one of 32 primary prostate cancer samples via PCR-SSCP.
- No mutations were identified in the p15, p18, or p19 genes using PCR-SSCP.
- Southern blot analysis revealed no structural alterations in any of the studied INK4 genes.
Conclusions:
- Structural abnormalities of INK4 CDKIs are infrequent in prostate carcinoma.
- Other mechanisms, such as gene methylation, may contribute to the loss of INK4 CDKI function in prostate cancer and warrant further study.