Role of Activating Transcription Factor 3 on TAp73 Stability and Apoptosis in Paclitaxel-Treated Cervical Cancer Cells

Taxol (paclitaxel) is a potent anticancer drug that has been found to be effective against several tumor types, including cervical cancer. However, the exact mechanism underlying the antitumor effects of paclitaxel is poorly understood. Here, paclitaxel induced the apoptosis of cervical cancer HeLa cells and correlated with the enhanced activation of caspase-3 and TAp73, which was strongly inhibited by TAp73B small interfering RNA (siRNA). In wild-type activating transcription factor 3 (ATF3) – overexpressed cells, paclitaxel enhanced apoptosis through increased A and B isoform expression of TAp73; however, these events were attenuated in cells containing inactive COOH-terminal – deleted ATF3 [ATF3(#C)] or ATF3 siRNA. In contrast, paclitaxel-induced ATF3 expression did not change in TAp73B-overexpressed or TAp73B siRNA – cotransfected cells. Furthermore,