ArticlePloS one2012
RCAN1 is an important mediator of glucocorticoid-induced apoptosis in human leukemic cells.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- PU.1 eviction at lymphocyte-specific chromatin domains mediates glucocorticoid response in acute lymphoblastic leukemia.Nature communications · 2024Article
- RCAN1-mediated calcineurin inhibition as a target for cancer therapy.Molecular medicine (Cambridge, Mass.) · 2022Review
- PTCH1-null induced pluripotent stem cells exclusively differentiate into immature ectodermal cells with large areas of medulloblastoma-like tissue.Discover oncology · 2022Article
- The long noncoding RNA HOTAIRM1 controlled by AML1 enhances glucocorticoid resistance by activating RHOA/ROCK1 pathway through suppressing ARHGAP18.Cell death & disease · 2021Article
- Article
- Sequential gene regulatory events leading to glucocorticoid-evoked apoptosis of CEM human leukemic cells:interactions of MAPK, MYC and glucocorticoid pathways.Molecular and cellular endocrinology · 2018Review
- Article
- Mechanisms of cyclic AMP/protein kinase A- and glucocorticoid-mediated apoptosis using S49 lymphoma cells as a model system.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Pituitary Adenylate Cyclase-activating Polypeptide (PACAP) Targets Down Syndrome Candidate Region 1 (DSCR1/RCAN1) to control Neuronal Differentiation.The Journal of biological chemistry · 2015Article
- The regulator of calcineurin (RCAN1) an important factor involved in atherosclerosis and cardiovascular diseases development.Journal of medicine and lifeReview
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucocorticoid (GC) is a major therapeutic agent for the treatment of leukemia because of its ability to induce apoptosis in lymphoid cells. The mechanism causing apoptosis, however, is still controversial. Since the glucocorticoid receptor is a transcription factor, some of its target genes are expected to be implicated in apoptosis. In this study, using a GC-sensitive human pre-B leukemia cell line, Nalm-6, the FK506 binding protein 51 (FKBP5) and regulator of calcineurin 1 (RCAN1) genes were disrupted by homologous recombination, since the expression of both is up-regulated by GC in GC-sensitive but not in GC-resistant leukemic cell lines. While the disruption of FKBP5 had a marginal effect on GC-induced apoptosis, that of RCAN1 resulted in marked resistance to GC. In addition, overexpression of RCAN1 rendered cells more sensitive to DEX. In RCAN1-disrupted cells, levels of some pro-apoptotic and anti-apoptotic Bcl-2 family proteins were decreased and increased, respectively. Finally, phosphorylation of cAMP-response element binding protein (CREB) and up-regulation of CREB target genes by GC were inhibited by RCAN1 disruption, and treatment with a cAMP-inducing agent, forskolin, restored the sensitivity to GC in RCAN1-disrupted Nalm-6 cells. These findings suggest that up-regulation of RCAN1 expression followed by activation of the CREB pathway is required in GC-induced apoptosis.
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