We examined the effect of suboptimal concentrations of cyclin-dependent kinase inhibitors, which do not interfere with cell proliferation, on retinoblastoma expression in hamster (Chinese hamster ovaryK1) and human (K562 and HeLa) cells. To achieve this, we used the chemical inhibitors roscovitine and olomoucine (which inhibit CDK2 prefer-entially),UCN-01 (which also inhibits CDK4/6) andp21 (as an intrinsic inhibitor). All chemical inhibitors and over-expression of p21 strongly induced retinoblastoma protein expression. UCN-01-mediated retinoblastoma expression was caused by an increase in both the levels of retino-blastoma mRNA and the stability of the protein
