P53-/- ve P53+/+ HCT116 kolon kanseri hücre serilerinde radyasyonun hücre proliferasyonu ce telomeraz aktivitesi üzerine etkisi
Özet
P53 is a tumor supressor protein and also known as ?Guardian of the Genome?. The p53 tumor supressor is a transcription factor that is activated by diverse genotoxic stresses. In response to variety types of DNA damage, the p53 tumor supresdsor gene product is activated and regulated number of downsteram cellular processes such as cell cycle arrest, apoptosis and DNA repair.The current study designed to response to radiation in the colon cancer cells in term of dependence on functional p53 activity. Studies were performed in p53 wild-type HCT116 cells and HCT116 cells with mutant p53. Exposure to 5 Gy gamma irradiation resulted in G1/S arrest in p53 wild-type cell lines, and in G2 phase arrest in p53-/- cell lines. These results suggest that p53 function alone does not control the progression of irradiated humon tumor cells from G1/S and G2/M. Telomerase activity is associated with p53 mutation. It is known that p53 is also a powerful inhibitor of human telomerase reverse transcriptase (hTERT) a key component for telomerase in the present study, we demonstrated that telomerase activity decreased in p53 +/+ cells whereas increased activity was detected in p53-/- HCT116 cells following exposure 5 Gy to ionizing radiation.
