PLC beta 1a and PLC beta 1b Selective Regulation and Cyclin D3 Modulation Reduced by Kinamycin F During K562 Cell Differentiation

Here we report that both PLC1a and PLC1b are relevant regulators of erythropoiesis in that kinamycin F, a potent inducer of -globin production in K562 cells, caused a selectively reduction of both PLC1 isozymes even though the results point out that the effect of the drug is mainly directed toward the expression of the PLC1a isoform. We have identified a different role for the two isozymes as regulators of K562 differentiation process induced by kinamycin F. The overexpression of PLC1b induced an increase in -globin expression even in the absence of kinamycin F. Moreover during K562 differentiation, cyclin D3 level is regulated by PLC1 signaling pathway. Namely the amplification of the expression of the PLC1a, but not of PLC1b, is able to maintain high levels of expression of cyclin D3 even after treatment with kinamycin F. This could be due to their different distribution in the cell compartments since the amount of PLC1b is mainly present in the nucleus in respect to PLC1a. Our data indicate that the amplification of PLC1a expression, following treatment with kinamycin F, confers a real advantage to K562 cells viability and protects cells themselves from apoptosis. J. Cell. Physiol. 230: 587-594, 2015. (c) 2014 Wiley Periodicals, Inc., A Wiley Company