Phosphoprotein B23 translocation and modulation of actinomycin D and doxorubicin cytotoxicity by dipyridamole in HeLa cells.

During continuous exposure, cells were more responsive to doxorubicin (DOX) in the presence of dipyridamole (DPM). Translocation of nucleolar phosphoprotein B23 and inhibition of cell growth occurred with a lower dose of DOX and in a shorter incubation time in the presence of DPM. DPM did not change translocation induced by actinomycin D (Act-D). Short exposure of HeLa cells to Act-D induced "reversible" translocation of protein B23 as well as "reversible" inhibition of cell growth. DPM included in the cell culture after removal of Act-D inhibited the recovery of cell growth as well as the corresponding relocalization of protein B23 from the nucleoplasm to nucleoli. DPM administered in the fresh medium after 30 min exposure to DOX had little effect on the potentiation of the induced translocation of protein B23 and inhibition of cell growth. Our results indicated that "B23 translocation" is closely associated with states of cell growth. The potentiation of the inhibition of cell growth by DPM is associated with the extent of enhanced protein B23 translocation. "B23 translocation" may therefore be a simple and rapid method for assessing the inhibition of cell growth and for determining the efficacy of combination cancer chemotherapy.