Vuletic, Ana (16243138800)Ana (16243138800)VuleticKonjevic, Gordana (56008692300)Gordana (56008692300)KonjevicMilanovic, Desanka (7004208324)Desanka (7004208324)MilanovicRuzdijic, Sabera (7003935669)Sabera (7003935669)RuzdijicJurisic, Vladimir (6603015144)Vladimir (6603015144)Jurisic2025-07-022025-07-022010https://doi.org/10.1007/s12253-009-9241-2https://www.scopus.com/inward/record.uri?eid=2-s2.0-77956886917&doi=10.1007%2fs12253-009-9241-2&partnerID=40&md5=ec11244b2bf8ac766fb59a3861edc013https://remedy.med.bg.ac.rs/handle/123456789/14111Retinoic acid (RA), similar to specific growth factors, can induce differentiation of proliferating promyelocytic precursors into terminally differentiated granulocytes, although little is known about effects of its 13-cis isomer on promyelocytic leukemia (PML). In this study we demonstrate that 13-cis-RA has a dose and time-dependant antiproliferative effect on HL-60 PML cell line, that it induces cell accumulation in resting G0/G1 phase of the cell cycle followed by an increase in CD11b granulocyte differentiation antigen expression. The obtained increase in the percentage of HL-60 cells in G0/G1 phase and complementary decrease in S phase of the cell cycle are accompanied by a decrease in the expression of cell cycle regulatory molecule cyclin B1. We also show the induction of interferon regulatory factor-1 (IRF-1) transcription that can, also, to some extent contribute to the antiproliferative effect of 13-cis-RA. Furthermore, down-regulation of Bcl-2 protein expression in 13-cis-RA treated HL-60 cells may contribute to sensitivity to apoptosis of growth arrested HL-60 promyelocytic cells. © 2010 Arányi Lajos Foundation.Cell cycleDifferentiationProliferationPromyelocytic leukemiaRetinoic acid