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Hepatocellular carcinoma (HCC) shows chemoresistant features to anticancer agents.Paclitaxel has been clinically used in the treatment of various cancers.However, HCC resisted the effects of paclitaxel on growth has not been adequately addressed.To investigate the effects and mechanisms of palitaxel on the growth of HCC, we performed experiments on HLE and Bel 7402 human hepatoma cells and L-02 human hepatocyte cells.MTT methods analyzed indicated that paclitaxel significantly inhibited the viability of HLE cells in a dose-and time-dependent manner, but did not affect Bel 7402 and L-02 cells; HLE cells resisted cytotoxicity ofpaclitaxel when transfected with pcDNA3.1-afp vectors; However,Bel 7402 cells sensitivity to paclitaxel were increased when transfected with AFP-siRNA.Paclitaxel significantly inhibited growth and enhanced apoptosis of HLE cells by inducing fragmentation of caspase-3 and inhibiting expression of Ras and Survivin, but pcDNA3.1-alp vectors been able to withstand these effects.However, paclitaxel could not promote fragmentation of caspase-3 and suppress expression of Ras and Survivin in Bel 7402 cells; Inhibited expression of AFP by AFP-siRNA maybe synergy paclitaxel to restrain growth and induced apoptosis, and enhance fragmantation of caspase-3 and repress expression of Ras and Survivin.Taken together, these results suggest that AFP may be an important factor against paclitaxel inhibited proliferation and induced apoptosis of HCC cells via repressing activity of caspase-3 and stimulating expression of Ras and Survivin in HCC cells; Target inhibited AFP expression synergism treated with paclitaxel were available strategy for therapeutic of HCC.