Abstract
Previous investigations have demonstrated the presence of conventional lipid kinases and phospholipase C (PLC) activities in nuclei of Friend erythroleukemia cells. Moreover, when Friend erythroleukemia cells are treated for 96 h with the antitumor drug tiazofurin, the induction of erythroid differentiation is accompanied by changes in amounts of both phosphatidylinositol and phosphatidylinositol 4,5-bisphosphate due to the inhibition of an uncharacterized nuclear PLC activity. Here, we show that the nuclear PLC β1 isoform is down-regulated by tiazofurin (5 µm) treatment of Friend erythroleukemia cells as shown by both Western blot and Northern blot analyses for PLC β1 message. This indicates that PLC β1 down-regulation is tightly linked with erythroid differentiation of Friend erythroleukemia cells and that the autonomous nuclear signaling via inositol lipid cycle can be controlled by the antitumor drug tiazofurin.
Footnotes
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↵1 This work was supported by Italian Consiglio Nazionale delle Ricerche Grants PF IG and PF ACRO and by AFRC International Scientific Interchange Scheme.
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↵2 To whom requests for reprints should be addressed.
- Received April 17, 1995.
- Accepted June 2, 1995.
- ©1995 American Association for Cancer Research.
Volume 55, Issue 14
