RADIATION-INDUCED APOPTOSIS IS NOT ENHANCED BY EXPRESSION OF EITHER P53 OR BAX IN SW626 OVARIAN-CANCER CELLS

The p53 protein is known to play a central role in mediating G(1) arre st or apoptosis in response to ionizing radiation in some cell types, It has been proposed that the Link between p53 and induction of apopto sis is provided in part by p53-mediated upregulation of BAX. In this s tudy, we used the human SW626 ovarian cancer cell line, which lacks fu nctional p53, to further investigate the relationship between wildtype p53, BAX, and apoptosis, SW626 cells expressing a temperature sensiti ve (ts) p53 mutant did not undergo G(1) arrest or apoptosis and did no t exhibit enhanced sensitivity to radiation at the permissive temperat ure of 32 degrees C, The tsp53 protein was functional in these cells a s evidenced by rapid induction of p21 at 32 degrees C, but not at 37 d egrees C, Interestingly, restoration of wildtype p53 function at 32 de grees C was not associated with BAS upregulation. In addition, stable overexpression of BAX in SW626 cells was not capable of enhancing apop totic cell death in response to radiation, Thus, failure of p53 to upr egulate BAS is not the sole reason for its inability to promote radiat ion-induced apoptosis in SW626 cells, Taken together, our data suggest that neither p53 nor BAX upregulation is sufficient for the induction of apoptosis in response to genotoxic damage in some cell types.