Molecular mechanism involved in TPA-induced myelopoietic programming.

The study, addressed to understand the mechanism responsible for 12-O-tetradecanoyl phorbol-13-acetate (TPA)-induced myeloid differentiation, revealed that the inherent capacity of TPA to induce expression of Receptor-C(K) in HL-60 cells (which are unable to express Receptor-C(K) in their native state) is responsible for its ability to induce phenotypic differentiation of HL-60 cells. Based upon these results, we propose that Receptor-C(K) dependent signalling is the Critical 'Molecular Switch' responsible for TPA-induced myelopoietic programming.