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Herceptin combined with carboplatin inhibiting cervical cancer cells and the related mechanism
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Abstract:
To evaluate the inhibitory effect of Herceptin on HeLa, SiHa cells and to investigate the synergistic mechanism of Herceptin and Carboplatin. Methods: HeLa and SiHa cells were treated with Herceptin (at 5, 10，20, 40, and 80 μg/ml), Carboplatin (at 0.5, 1, 2, 4, and 8 μg/ml), and Her＋CBP\[（10＋1), (20＋2), and (40＋4) μg/ml\] separately. The untreated cells were taken as control. SP immunohistochemical method was used to detect the protein expression of HER2/neu and downstream Ras oncogene. MTT method was used to study the inhibition effect of Herceptin on HeLa, SiHa cells and its synergetic effect with carboplatin. FCM was used to detect the cell apoptosis and cell cycle. The mRNA expression of her2/neu and ras were assessed by RTPCR；the protein expression of HER2/neu and Ras were studied by Western blotting. Results: Herceptin significantly inhibited cervical cancer cells proliferation, and there was a synergistic effect when combined with carboplatin (P＜0.05, P＜0.01).Herceptin induced cell apoptosis and arrested cell at G1 phase. When combined with Carboplatin, Herceptin induced more severe apoptosis and arrested cell at G2 phase; meanwhile, the cells of S and also decreased. The mRNA and protein expressions of HER2/neuand Ras were decreased after treated with Herceptin alone and in combination with Carboplatin (P＜0.05). The inhibitory effect of Herceptin and Carboplatin was more obvious on HeLa cells. Conclusion: Herceptin alone or in combination with Carboplatin can greatly inhibit the growth to HeLa and SiHa cells. The synergistic mechanism of Herceptin with Carboplatin is related to the double blockage of cell cycle. The inhibitory effect is more obvious on HeLa cells. Herceptin inhibits proliferation of cervical cancer cells by restraining Ras/MAPK pathway.
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Clc Number:
R737.9
