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Mechanisms of all-trans retinoic acid-induced differentiation of acute promyelocytic leukemia cells Zhang JW; Wang JY; Chen SJ; Chen ZJ Biosci 2000[Sep]; 25 (3): 275-84Retinoic acids (RA) play a key role in myeloid differentiation through their agonistic nuclear receptors (RAR alpha/RXR) to modulate the expression of target genes. In acute promyelocytic leukemia (APL) cells with rearrangement of retinoic acid receptor a (RAR alpha) (including: PML-RAR alpha, PLZF-RAR alpha, NPM-RAR alpha, NuMA- RAR alpha or STAT5b-RAR alpha) as a result of chromosomal translocations, the RA signal pathway is disrupted and myeloid differentiation is arrested at the promyelocytic stage. Pharmacologic dosage of all-trans retinoic acid (ATRA) directly modulates PML-RAR alpha and its interaction with the nuclear receptor co-repressor complex, which restores the wild-type RAR alpha/RXR regulatory pathway and induces the transcriptional expression of downstream genes. Analysing gene expression profiles in APL cells before and after ATRA treatment represents a useful approach to identify genes whose functions are involved in this new cancer treatment. A chronologically well coordinated modulation of ATRA-regulated genes has thus been revealed which seems to constitute a balanced functional network underlying decreased cellular proliferation, initiation and progression of maturation, and maintenance of cell survival before terminal differentiation.|Antineoplastic Agents/*pharmacology/therapeutic use[MESH]|Cell Differentiation/*drug effects[MESH]|Gene Expression Regulation, Leukemic/*drug effects[MESH]|HL-60 Cells/cytology/drug effects[MESH]|Humans[MESH]|Leukemia, Promyelocytic, Acute/drug therapy/genetics/*pathology[MESH]|Neoplasm Proteins/*drug effects/genetics/physiology[MESH]|Nuclear Proteins/physiology[MESH]|Nuclear Receptor Co-Repressor 1[MESH]|Oncogene Proteins, Fusion/*drug effects/genetics[MESH]|Receptors, Retinoic Acid/*agonists/genetics/physiology[MESH]|Repressor Proteins/physiology[MESH]|Retinoic Acid Receptor alpha[MESH]|Retinoid X Receptors[MESH]|Signal Transduction/drug effects[MESH]|Transcription Factors/physiology[MESH]|Transcription, Genetic/drug effects[MESH]|Translocation, Genetic[MESH]|Tretinoin/*pharmacology/therapeutic use[MESH]|Tumor Cells, Cultured/cytology/drug effects[MESH] |
