Induction of CXC and CC chemokines by all-trans retinoic acid in acute promyelocytic leukemia cells

Shibakura, Misako; Niiya, Kenji; Niiya, Masami; Asaumi, Noboru; Yoshida, Chie; Nakata, Yasunari; Tanimoto, Mitsune

doi:10.1016/j.leukres.2005.01.005

Cited by 27 publications

(32 citation statements)

References 14 publications

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Section: Discussionmentioning

confidence: 95%

“…It was thus possible that another retinoid-related signaling pathway was involved in the transcriptional regulation of CYP26A1. For instance, chemokine production has been linked to ATRA sensitivity, [39][40][41] we consequently investigated the possibility that maturation events play a role in enhancing ATRA metabolism.…”

Section: Apl Blast Sensitivity Correlates With the Transcriptional Ramentioning

confidence: 99%

“…In addition, chemokine production has previously been linked to ATRA sensitivity and is thought to be involved in the leukocyte activation events that occur along with differentiation. [39][40][41] Moreover, in NB4 cells, we obtained evidence that a novel signaling pathway is activated in APL cells on ATRA treatment, whereby interleukin-8 activates CYP26A1 transcription by inducing the specific transactivation of the HOXA10v2 factor.The balance between influx and efflux rates determined the effective cellular uptake of retinoid in target cells. Metabolism occurred through microsomal membrane-bound p450 cytochromes and involved the hydroxylation of the ligand and the extracellular efflux of catabolite forms 42 that are impoverished in their differentiation efficiency.…”

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confidence: 95%

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Pharmacogenomic analysis of acute promyelocytic leukemia cells highlights CYP26 cytochrome metabolism in differential all-trans retinoic acid sensitivity

Quéré

Baudet

Cassinat

et al. 2007

Blood

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Disease relapse sometimes occurs after acute promyelocytic leukemia (APL) therapy with all-trans retinoic acid (ATRA). Among the diagnostic parameters predicting relapse, heterogeneity in the in vitro differentiation rate of blasts is an independent factor. To identify biologic networks involved in resistance, we conducted pharmacogenomic studies in APL blasts displaying distinct ATRA sensitivities. Although the expression profiles of genes invested in differentiation were similarly modulated in low-and high-sensitive blasts, low-sensitive cells showed higher levels of transcription of ATRA-target genes, transcriptional regulators, chromatin remodelers, and transcription factors. In opposition, only high-sensitive blasts expressed the CYP26A1 gene, encoding the p450 cytochrome which is known to be involved in retinoic acid catabolism. In NB4 cells, ATRA treatment activates a novel signaling pathway, whereby interleukin-8 stimulates the expression of the homeobox transcription factor HOXA10v2, an effective enhancer of CYP26A1 transcription. These data were corroborated in primary APL cells, as maturation levels correlated with CYP26A1 expression. IntroductionHematopoiesis can be described as a balance between proliferation and differentiation. In 90% of acute promyelocytic leukemia (APL) cases, the t(15;17) translocation and consequent expression of the PML (promyelocytic leukemia protein)/RAR␣ (retinoic acid receptor ␣) fusion protein blocks differentiation at the promyelocytic stage. RAR␣ belongs to the nuclear receptor superfamily and functions as a ligand-dependent transcription factor, acting to establish the granulocytic lineage. Under normal conditions, binding of the ligand (all-trans retinoic acid, or ATRA) to the receptor provokes a conformational change in the receptor resulting in the disruption of a co-repression complex, recruitment of coactivators, binding to the retinoic acid response element (RARE), and finally the transcription of ATRA-dependent genes. 1 The PML portion of the PML/RAR␣ fusion protein has a high affinity for the corepression complex, preventing RAR␣ transcriptional activity. To induce complete remission in a high proportion of patients, a pharmacologic dose of ATRA is required to destabilize this interaction and reestablish the differentiation program. Combining ATRA with chemotherapy results in a significant prolongation of disease-free and overall survival. [2][3][4][5][6] Despite the general efficacy of ATRA-based therapy, 10% to 20% of patients with APL still relapse. Several mechanisms have been proposed to explain the involved retinoid resistance arising during cancer therapy. With the exception of primary resistance, which is extremely rare in PML/RAR␣ cells, 7,8 APL relapse has been suggested to be related to various processes observed in cell lines. These include variations in nuclear ATRA concentrations due to, for example, cytoplasm retinoid sequestration, 9,10 increased intracellular metabolism, 11 alterations in ATRA transcriptional efficiency via mutations in the P...

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Section: Discussionmentioning

confidence: 95%

Section: Apl Blast Sensitivity Correlates With the Transcriptional Ramentioning

confidence: 99%

mentioning

confidence: 95%

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Pharmacogenomic analysis of acute promyelocytic leukemia cells highlights CYP26 cytochrome metabolism in differential all-trans retinoic acid sensitivity

Quéré

Baudet

Cassinat

et al. 2007

Blood

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“…Previously, it has been observed that differentiation therapy in acute promyelocytic leukemia (APL) (1) increases the release of inflammatory cytokines from differentiating APL cells, 3 (2) increases the expression of cellular adhesion molecules on leukocytes, 4 and (3) up-regulates specific chemokines. 5 The simultaneous production of these proteins after exposure to all-trans retinoic acid (ATRA) may exacerbate the hyperinflammation observed in DS. The incidence of DS in patients receiving ATRA/arsenic trioxide (ATO) treatment has been reported to range from 2% to 27% with an associated mortality of about 2%.…”

Section: Ccl2/ccr2: Push/pull For Migration -------------------------mentioning

confidence: 99%

“…[4][5][6] The Seattle group has been in the vanguard of the development of reduced-intensity transplantation preparative regimens. 7 It is notable that the patients treated by Pagel et al were deemed ineligible for their standard reduced-intensity preparative regimen of fludarabine and TBI alone.…”

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confidence: 99%

CCL2/CCR2: push/pull for migration

Avvisati

2009

Blood

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Overview of retinoid metabolism and function

2006

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Retinoids (vitamin A) are crucial for most forms of life. In chordates, they have important roles in the developing nervous system and notochord and many other embryonic structures, as well as in maintenance of epithelial surfaces, immune competence, and reproduction. The ability of all-trans retinoic acid to regulate expression of several hundred genes through binding to nuclear transcription factors is believed to mediate most of these functions. The role of all-trans retinoic may extend beyond the regulation of gene transcription because a large number of noncoding RNAs also are regulated by retinoic acid. Additionally, extra-nuclear mechanisms of action of retinoids are also being identified. In organisms ranging from prokaryotes to humans, retinal is covalently linked to G protein-coupled transmembrane receptors called opsins. These receptors function as light-driven ion pumps, mediators of phototaxis, or photosensory pigments. In vertebrates phototransduction is initiated by a photochemical reaction where opsin-bound 11-cis-retinal is isomerized to all-trans-retinal. The photosensitive receptor is restored via the retinoid visual cycle. Multiple genes encoding components of this cycle have been identified and linked to many human retinal diseases. Central aspects of vitamin A absorption, enzymatic oxidation of all-trans retinol to all-trans retinal and all-trans retinoic acid, and esterification of all-trans retinol have been clarified. Furthermore, specific binding proteins are involved in several of these enzymatic processes as well as in delivery of all-trans retinoic acid to nuclear receptors. Thus, substantial progress has been made in our understanding of retinoid metabolism and function. This insight has improved our view of retinoids as critical molecules in vision, normal embryonic development, and in control of cellular growth, differentiation, and death throughout life.

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Induction of CXC and CC chemokines by all-trans retinoic acid in acute promyelocytic leukemia cells

Cited by 27 publications

References 14 publications

Pharmacogenomic analysis of acute promyelocytic leukemia cells highlights CYP26 cytochrome metabolism in differential all-trans retinoic acid sensitivity

Pharmacogenomic analysis of acute promyelocytic leukemia cells highlights CYP26 cytochrome metabolism in differential all-trans retinoic acid sensitivity

CCL2/CCR2: push/pull for migration

Overview of retinoid metabolism and function

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