Abstract: To study the effects of cisplatin on the expression of downstream signal factors of the p53 pathway in gastric cancer cell lines with wild-type p53 (AGS cell) or mutated p53 (MGC-803, SGC-7901 cells), and to explore its mechanism. MethodsAGS, MGC-803 and SGC-7901 cells were treated with different concentrations of cisplatin (0μg/mL, 1μg/mL and 2μg/mL) for 24 hours. (1) FCM was used to determine the percentage of cells in each cell cycle phase and the apoptosis rate． (2) Reverse transcription-polymerase chain reaction (RT-PCR) was used to determine the expression changes of downstream signal factors of the p53 pathway including p21, bax, puma, bcl-2 and bcl-xl. Results(1) After treatment with cisplatin， the number of cells in phase S+G2 was obviously increased in all three types of cells, and the apoptosis rate was also manifested (P<0.01)． (2) After cisplatin treatment, in AGS cells, p53, bax and p21 were increased in a dose-dependent fashion (P<0.05), puma had no significant changes, while the expressions of bcl-2 and bcl-xl decreased with the increase of the cisplatin dose (P<0.05), also in MGC-803 and SGC-7901 cells, the expressions of bcl-2 and bcl-xl were decreased with the increase of the concentration of cisplatin, while bax, p21 and puma had no significant changes. ConclusionsIn p53 mutated gastric cancer cells, the damage of DNA could still arrest the cell cycle phase and leads to apoptosis, with expression changes of apoptosis signal factors.
This mechanism may be due to the specific mutated sites of p53 transmitting signals of DNA damages downward to apoptosis factors, or perhaps due to the p53 independent pathway that is not disturbed by p53 mutation.

Key words: Gene p53, Gastric cancer cell, Cisplatin