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Archive > Volume 20 Issue 2 > 2013,20(2):192-196. DOI:10.3872/j.issn.1007-385X.2013.02.011 Prev Next
Basic Research
Inhibitory effect of recombinant human adenovirus- P53 combined with paclitaxel on human cervical cancer HeLa cells and its mechanism
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Abstract:
Objective: To evaluate the effect of recombinant human adenovirus- P53 (rAd-P53) combined with paclitaxel on proliferation, apoptosis and vascular endothelial growth factor (VEGF) expression of cervical cancer HeLa cells. Methods: The effects of paclitaxel, rAd-P53 alone or in combination on the proliferation of HeLa cells were evaluated by MTT. The effects of paclitaxel, rAd-P53 alone or in combination on apoptosis of HeLa cells at 48 h were evaluated by DAPI stain. The effects of paclitaxel, rAd-P53 alone or in combination on VEGF expression in HeLa cells were examined by Western blotting. Results: Paclitaxel, rAd-P53 alone or in combination inhibited HeLa cell proliferation significantly at 24-72 h in dose-dependent and time-dependent manners. Furthermore, the inhibitory effect was more significant with rAd-P53 combined with paclitaxel than with paclitaxel or rAd-P53 alone group (P<0.05). The coefficients of drug interaction (CDI) of various doses of rAd-P53 combined with paclitaxel were less than 1, which indicated that there was a synergism between them. At 48 h of treatment, rAd-P53 (5×107 VP/ml) combined with paclitaxel (3 μg/ml) showed stronger cell inhibition than the two drugs treated alone (\[54.0 ± 0.92\]% vs \[31.8 ± 0.58\]%, \[27.2±0.55\]%, P<0.05). In addition, the combined group demonstrated more powerful ability in apoptosis induction than paclitaxel and rAd-P53 alone（ \[83±0.07\]% vs \[36±0.04\]%,\[62±0.05\]%，P<0.05), but the expression of VEGF in HeLa cells in the combined treatment group decreased more significantly than did the single drug groups (\[81 ± 0.08\]% vs \[45±0.07\]%, \[60±0.06\]%, P<0.05). Conclusion: rAd-P53 combined with paclitaxel shows more significant proliferation inhibition and apoptosis induction effects than does paclitaxel or rAd-P53 alone. Its mechanism may be associated with down-regulation of VEGF expression.
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Project Supported:
Project supported by the Kanglaite Clinical Cancer Research Foundation from Health Bureau of Jiangsu Province （No. P200943）
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