Phorbol ester stimulated Cip1 expression in p53-negative leukemic cells
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- Published online on: January 1, 1996 https://doi.org/10.3892/or.3.1.213
- Pages: 213-217
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Abstract
In differentiating leukemic cells, cyclin-dependent kinase interacting protein (Cip1) is induced and stimulates a G(1) arrest. TPA treated U937 monoblastoid cells expressed Cip1, hypophosphorylated retinoblastoma protein (Rb), arrested in G(1) and differentiated. PKC-zeta cells are U937 cells that overexpress the zeta isoform and display alterations in endogenous PKC isoform expression. TPA treated PKC-zeta cells undergo apoptosis without differentiating. TPA treated PKC-zeta cells express Cip1 and display substantial hypophosphorylation of Rb but fail to arrest in G(1). Thus, a novel phorbol ester dependent signalling pathway exists in which Cip1 induction is associated with the absence of a G(1) arrest and induction of apoptosis rather than differentiation.
