Point mutations in codon 12 and 13 of K-ras are frequently found in DNA of colorectal cancer. It has beensuggested that particular mutations at these sites may be associated with specific tumour phenotypes. To shed lighton the molecular mechanisms on which depends this specificity we set up a system of HT-29 cells stablytransfected with a cDNA coding for K-rasG13D under the control of an inducible promoter. Proliferation assayperformed on one of the positives clones, showed a decreased growth rate in response to K-rasG13D expressionand preliminary gene expression analysis showed an up-regulation of the cell-cycle inhibitor p21 WAF1.
|Numero di pagine||3|
|Stato di pubblicazione||Published - 2010|