Involvement of PKC in TPA-potentiated apoptosis induction during hemin-mediated erythroid differentiation in K562 cells.

Triggering differentiation has been employed as a strategy to inhibit cell proliferation and accelerate apoptosis in malignant cells. To better understand the mechanisms underlying differentiation-mediated regulation of apoptosis, we have studied the effects of PKC pathway with an activator of the protein kinase C, 12-O-tetradecanoylphorbol-13-acetate (TPA), during hemin-induced erythroid differentiation of K562 erythroleukemia cells. K562 cell line has been used as a model of common progenitor of erythroblasts and magakaryocytes and can be differentiated into erythroid and megakaryocytic lineages by hemin and TPA, respectively.

Involvement of nPKC-MAPK pathway in the decrease of nucleophosmin/B23 during megakaryocytic differentiation of human myelogenous leukemia K562 cells.

Human myelogenous leukemia K562 cells were induced to undergo megakaryocytic differentiation by long-term treatment with phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate (TPA). The protein level of nucleophosmin/B23 (NPM/B23), a nucleolar protein, was substantially decreased upon TPA treatment. In this study, we found that the proteasome inhibitors blocked the decrease of NPM/B23 protein in response to TPA, suggesting the proteasomes were involved in the downregulation of NPM/B23 upon megakaryocytic differentiation.