ArticleCancer science2007
Active FKHRL1 overcomes imatinib resistance in chronic myelogenous leukemia-derived cell lines via the production of tumor necrosis factor-related apoptosis-inducing ligand.
Article in Cancer science, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.
- BCR-ABL-mediated upregulation of PRAME is responsible for knocking down TRAIL in CML patients.Oncogene · 2011Pooled it
- Uncovering the Molecular Pathways Implicated in the Anti-Cancer Activity of the Imidazoquinoxaline Derivative EAPB02303 Using aInternational journal of molecular sciences · 2024Article
- aPKC controls endothelial growth by modulating c-Myc via FoxO1 DNA-binding ability.Nature communications · 2018Article
- Critical role of FOXO3a in carcinogenesis.Molecular cancer · 2018Review
- Transcription factors FOXO in the regulation of homeostatic hematopoiesis.Current opinion in hematology · 2018Review
- Bcl6 gene-silencing facilitates PMA-induced megakaryocyte differentiation in K562 cells.Journal of cell communication and signaling · 2017Article
- FOXO Signaling Pathways as Therapeutic Targets in Cancer.International journal of biological sciences · 2017Review
- Identification of FOXM1 as a therapeutic target in B-cell lineage acute lymphoblastic leukaemia.Nature communications · 2015Article
- BRCA1-IRIS inactivation overcomes paclitaxel resistance in triple negative breast cancers.Breast cancer research : BCR · 2015Article
- The antiproliferative activity of kinase inhibitors in chronic myeloid leukemia cells is mediated by FOXO transcription factors.Stem cells (Dayton, Ohio) · 2014Article
- STI571 reduces TRAIL-induced apoptosis in colon cancer cells: c-Abl activation by the death receptor leads to stress kinase-dependent cell death.Journal of biomedical science · 2012Article
- Computational identification and modeling of crosstalk between phosphorylation, O-β-glycosylation and methylation of FoxO3 and implications for cancer therapeutics.International journal of molecular sciences · 2012Article
- The Interface between BCR-ABL-Dependent and -Independent Resistance Signaling Pathways in Chronic Myeloid Leukemia.Leukemia research and treatment · 2012Article
- Loss of memory B cells during chronic HIV infection is driven by Foxo3a- and TRAIL-mediated apoptosis.The Journal of clinical investigation · 2011Article
- Bimodal regulation of FoxO3 by AKT and 14-3-3.Biochimica et biophysica acta · 2011Article
- Isotretinoin and FoxO1: A scientific hypothesis.Dermato-endocrinology · 2011Article
- Protein S blocks the extrinsic apoptotic cascade in tissue plasminogen activator/N-methyl D-aspartate-treated neurons via Tyro3-Akt-FKHRL1 signaling pathway.Molecular neurodegeneration · 2011Article
- Novel avenues of drug discovery and biomarkers for diabetes mellitus.Journal of clinical pharmacology · 2011Review
- Resveratrol induces growth arrest and apoptosis through activation of FOXO transcription factors in prostate cancer cells.PloS one · 2010Article
- Abelson virus transformation prevents TRAIL expression by inhibiting FoxO3a and NF-kappaB.Molecules and cells · 2010Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FKHRL1 (also called FOXO3a) is a member of the Forkhead Box, class O (FOXO) subfamily of forkhead transcription factors and functions downstream of Bcr-Abl tyrosine kinase as a phosphorylated inactive form in chronic myelogenous leukemia (CML). The Bcr-Abl tyrosine kinase inhibitor imatinib induces cell cycle arrest and subsequent apoptosis via the conversion of FKHRL1 from the phosphorylated inactive form to the dephosphorylated active form in CML-derived cell lines. In the present study, we examined whether active FKHRL1 can overcome resistance to imatinib. To this end, we generated a 4-hydroxytamoxifen-inducible active FKHRL1 (FKHRL1-TM; a triple mutant of FKHRL1 in which all three Akt phosphorylation sites have been mutated)-estrogen receptor fusion protein expression system in CML-derived imatinib-resistant cell lines. 4-Hydroxytamoxifen inhibited cell growth and cell cycle progression, and subsequently induced apoptosis, accompanied by upregulation of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Thus, active FKHRL1 antagonized deregulated proliferation and induced apoptosis in these cell lines. In addition, imatinib-resistant cells underwent apoptosis after transfection with full-length TRAIL cDNA. Collectively, our results suggest that active FKHRL1 can overcome imatinib resistance in CML cells, in part via TRAIL production.
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