Development of resistance to one type of lipophilic chemotherapeutic drug often leads to resistance to other, structurally unrelated, lipophilic drugs. This suggests that non-toxic lipophilic agents may interfere with and reverse drug resistance by saturating the pathway through which multidrugresis
Phosphoprotein B23 translocation and modulation of actinomycin D and doxorubicin cytotoxicity by dipyridamole in hela cells
โ Scribed by Amy Meei-Shuu Bor; Fu-Jung Chang; Benjamin Yat-Ming Yunc
- Publisher
- John Wiley and Sons
- Year
- 1992
- Tongue
- French
- Weight
- 688 KB
- Volume
- 52
- Category
- Article
- ISSN
- 0020-7136
No coin nor oath required. For personal study only.
โฆ Synopsis
During continuous exposure, cells were more responsive to doxorubicin (DOX) in the presence of dipyridamole (DPM). Translocation of nucleolar phosphoprotein 823 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 823 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 823 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 823 and inhibition of cell growth. Our results indicated that "823 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 823 translocation. "823 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.
๐ SIMILAR VOLUMES