The analysis of checkpoint mechanism of cell cycle in liver cancer cells

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Using gene targeting with AAV vectors, we established hetero knock-out HepG2 cells clones (p53+/-) of which Exon2 in endogeneous TP53 alleles were destroyed. However, TP53 homo knock-out HepG2 cells clones have not been obtained. These results derived a hypothesis that p53 might be essential for cell proliferation in HepG2 cells, but knock down of expression of p53 using siRNA did not decrease cell proliferation.On the other hand, we found that p53+/- cells constantly expressed deltaN40p53, an isoform of p53. Since the function of deltaN40p53 has been known little in liver cancer, we investigated the function of deltaN40p53 in HepG2 cells by using several methods. Our studies revealed that deltaN40p53 enhanced the expression of p21 and induced an increase of G1/S arrest, that is, deltaN40p53 made up for the function of p53 and suppressed tumor cell proliferation and induced cellular senescence in HepG2 cells when the expression of p53 was reduced.