PMID- 9016759 OWN - NLM STAT- MEDLINE DCOM- 19970305 LR - 20181130 IS - 0006-291X (Print) IS - 0006-291X (Linking) VI - 230 IP - 2 DP - 1997 Jan 13 TI - Possible involvement of Bcl-2 pathway in retinoid X receptor alpha-induced apoptosis of HL-60 cells. PG - 251-3 AB - Retinoids induce granulocytic differentiation and subsequent apoptosis in human myeloid (HL-60) leukemia cells. Differentiation is induced due to activation of retinoic acid receptors (RARs) whereas, activation of retinoid X receptors (RXRs) seems to be essential for driving these cells into apoptosis. In order to understand the mechanism of RXR induced apoptosis, we used a variant HL-60 cell line (HL-60R) with a transdominant negative mutation. The retroviral vector-mediated gene transfer was used to introduce the functional RARs or RXR alpha into HL-60R cells. We studied the effect of receptor-selective retinoid treatment on the expression of Bcl-2 and Bax oncogenes by reverse-transcription polymerase chain reaction (RT-PCR) and immunoblot analysis in RARs and RXR alpha transfected HL-60 cells. Our results show that activation of RXR alpha results in apoptosis via down-modulation of Bcl-2 mRNA as well as its gene product expression with no change in Bax mRNA expression. FAU - Agarwal, N AU - Agarwal N AD - Department of Anatomy and Cell Biology, University of North Texas Health Science Center and North Texas Eye Research Institute, Fort Worth 76107, USA. nagarwal@molly.hsc.unt.edu FAU - Mehta, K AU - Mehta K LA - eng PT - Journal Article PL - United States TA - Biochem Biophys Res Commun JT - Biochemical and biophysical research communications JID - 0372516 RN - 0 (BAX protein, human) RN - 0 (Proto-Oncogene Proteins) RN - 0 (Proto-Oncogene Proteins c-bcl-2) RN - 0 (RARA protein, human) RN - 0 (Receptors, Retinoic Acid) RN - 0 (Recombinant Proteins) RN - 0 (Retinoic Acid Receptor alpha) RN - 0 (Retinoid X Receptors) RN - 0 (Transcription Factors) RN - 0 (bcl-2-Associated X Protein) RN - 1UA8E65KDZ (Alitretinoin) RN - 5688UTC01R (Tretinoin) SB - IM MH - Alitretinoin MH - *Apoptosis MH - HL-60 Cells MH - Humans MH - Mutation MH - Oncogenes MH - Polymerase Chain Reaction MH - Proto-Oncogene Proteins/biosynthesis MH - Proto-Oncogene Proteins c-bcl-2/*biosynthesis MH - Receptors, Retinoic Acid/biosynthesis/*physiology MH - Recombinant Proteins/biosynthesis MH - Retinoic Acid Receptor alpha MH - Retinoid X Receptors MH - Retroviridae MH - Transcription Factors/biosynthesis/*physiology MH - *Transcription, Genetic/drug effects MH - Transfection MH - Tretinoin/*pharmacology MH - bcl-2-Associated X Protein EDAT- 1997/01/13 00:00 MHDA- 1997/01/13 00:01 CRDT- 1997/01/13 00:00 PHST- 1997/01/13 00:00 [pubmed] PHST- 1997/01/13 00:01 [medline] PHST- 1997/01/13 00:00 [entrez] AID - S0006-291X(96)95937-9 [pii] AID - 10.1006/bbrc.1996.5937 [doi] PST - ppublish SO - Biochem Biophys Res Commun. 1997 Jan 13;230(2):251-3. doi: 10.1006/bbrc.1996.5937.