Tumor necrosis factor-related apoptosis inducing ligand overexpression and Taxol treatment suppresses the growth of cervical cancer cells in vitro and in vivo.

Tumor necrosis factor-related apoptosis inducing ligand (TRAIL) is a member of tumor necrosis factor (TNF) superfamily and functions to promote apoptosis by binding to cell surface death receptor (DR)4 and DR5. Cancer cells are more sensitive than normal cells to TRAIL-induced apoptosis, and TRAIL-based therapeutic strategies have shown promise for the treatment of cancer. The present study investigated whether enforced overexpression of TRAIL in cervical cancer cells promoted cell death in the presence or absence of Taxol, an important first-line cancer chemotherapeutic drug. Hela human cervical cancer cells were transfected with a TRAIL expression plasmid, and the effects of the combination treatment with Taxol on apoptosis was investigated in vitro and in tumor xenografts in vivo. The results indicated that Taxol treatment and TRAIL overexpression enhanced apoptosis compared with either treatment alone. The present data indicate that Taxol may enhance the pro-apoptotic effects of TRAIL overexpression in HeLa cells by increasing cleaved caspase-3 and DR5 expression levels and decreasing Bcl-2 expression levels. Furthermore, the findings suggest a possible novel treatment option for cervical cancer and uncovers a potential mechanism of the enhancing effects of Taxol on TRAIL-induced apoptosis.