Transforming growth factor-beta1 induces junB mRNA accumulation, G1-phase arrest, and pRb dephosphorylation in human leukemia HL-60 cells.

Although TGF-beta1 unambiguously functions as a regulator of hematopoietic differentiation, its significance for the development of myeloid lineage is still questionable. In this study three components of early response to TGF-beta1 treatment were investigated in human promyelocytic leukemia HL-60 cells. Changes in junB mRNA accumulation and pRb dephosphorylation were accompained by accumulation of cells in G1 phase of the cell cycle. Time dependence of these changes may implicate mutual cooperation of the pRb and junB in the cell cycle control. It can be concluded that, although myeloid HL-60 cells are known to require rather complex cytokine stimulation to fully differentiate, they clearly possess the ability to respond to TGF-beta1.