P15——a new tumor suppressor gene

In addition to the tumor suppressor genes such as Rb and p53, it has been found that some molecules of the same class named CKI (cyclin-dependent kinase inhibitor) also play an important role in the inhibition of tumorigenesis and the tumor progression. In the KIP and INK4 families of CKIs, p15 shares extensive homology with p16. Findings in many tumors and their cell lines show that the inactivation of p15 (deletion, mutation, rearrangement, etc.) is very frequent, and inactive p15 is involved in the progress of some tumors. These studies provide evidence that the p15 is a new tumor suppressor gene. Furthermore, the research on the molecular mechanism of p15 in regulation of cell proliferation shows that p15 can inhibit the growth of some kinds of tumor cells, and p15 is the mediator of TGF-β-induced cell arrest. Investigations on p15 in cell differentiation suggest that increased p15 is related to the change of malignant phenotype. These results supply clues for further interpretation about the molecular mechnism of cell cycle control and cell tumorigenesis. And they may provide theoretical and experimental basis for application of p15 to clinical therapy of tumors.

P15—A new tumor suppressor gene

In addition to the tumor suppressor genes such asRb andp53, it has been found that some molecules of the same class named CKI (cyclin-dependent kinase inhibitor) also play an important role in the inhibition of tumorigenesis and the tumor progression. In the KIP and INK4 families of CKls,p15 shares extensive homology withp16. Findings in many tumors and their cell lines show that the inactivation ofp15 (deletion, mutation, rearrangement, etc.) is very frequent, and inactivep15 is involved in the progress of some tumors. These studies provide evidence that thep15 is a new tumor suppressor gene. Furthermore, the research on the molecular mechanism ofp15 in regulation of cell proliferation shows thatp15 can inhibit the growth of some kinds of tumor cells, andp15 is the mediator of TGF-β-induced cell arrest. Investigations onp15 in cell differentiation suggest that increasedp15 is related to the change of malignant phenotype. These results supply clues for further interpretation about the molecular mechnism of cell cycle control and cell tumorigenesis. And they may provide theoretical and experimental basis for application ofp15 to clinical therapy of tumors.