ArticleLeukemia2007
Identification of TSC-22 as a potential tumor suppressor that is upregulated by Flt3-D835V but not Flt3-ITD.
Article in Leukemia, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Regulation of Alternative Polyadenylation Events by PABPC1 Affects Erythroid Progenitor Cell Expansion.Genomics, proteomics & bioinformatics · 2025Article
- RNA-binding protein MEX3D promotes cervical carcinoma tumorigenesis by destabilizing TSC22D1 mRNA.Cell death discovery · 2022Article
- Identification of novel CEBPA double mutations capable of promoting familial AML via the suppression of myeloid differentiation.American journal of translational research · 2020Article
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- Human CD300C delivers an Fc receptor-γ-dependent activating signal in mast cells and monocytes and differs from CD300A in ligand recognition.The Journal of biological chemistry · 2013Article
- Establishment and Validation of an Orthotopic Metastatic Mouse Model of Colorectal Cancer.ISRN hepatology · 2013Article
- Aberrant expression of RasGRP1 cooperates with gain-of-function NOTCH1 mutations in T-cell leukemogenesis.Leukemia · 2012Article
- Subcellular TSC22D4 localization in cerebellum granule neurons of the mouse depends on development and differentiation.Cerebellum (London, England) · 2012Article
- Regulation of TGF-β signaling by PKC depends on Tsc-22 inducibility.Molecular and cellular biochemistry · 2012Article
- Transforming growth factor-β-stimulated clone-22 is a negative-feedback regulator of Ras / Raf signaling: Implications for tumorigenesis.Cancer science · 2012Article
- Differential signaling of Flt3 activating mutations in acute myeloid leukemia: a working model.Protein & cell · 2011Review
- Transforming Growth Factor-{beta}-Stimulated Clone-22 Is an Androgen-Regulated Gene That Enhances Apoptosis in Prostate Cancer following Insulin-Like Growth Factor-I Receptor Inhibition.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009Article
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- The Drosophila homolog of human tumor suppressor TSC-22 promotes cellular growth, proliferation, and survival.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor-beta (TGF-beta)-stimulated clone-22 (TSC-22) was originally isolated as a TGF-beta-inducible gene. In this study, we identified TSC-22 as a potential leukemia suppressor. Two types of FMS-like tyrosine kinase-3 (Flt3) mutations are frequently found in acute myeloid leukemia: Flt3-ITD harboring an internal tandem duplication in the juxtamembrane domain associated with poor prognosis and Flt3-TKD harboring a point mutation in the kinase domain. Comparison of gene expression profiles between Flt3-ITD- and Flt3-TKD-transduced Ba/F3 cells revealed that constitutive activation of Flt3 by Flt3-TKD, but not Flt3-ITD, upregulated the expression of TSC-22. Importantly, treatment with an Flt3 inhibitor PKC412 or an Flt3 small interfering RNA decreased the expression level of TSC-22 in Flt3-TKD-transduced cells. Forced expression of TSC-22 suppressed the growth and accelerated the differentiation of several leukemia cell lines into monocytes, in particular, in combination with differentiation-inducing reagents. On the other hand, a dominant-negative form of TSC-22 accelerated the growth of Flt3-TKD-transduced 32Dcl.3 cells. Collectively, these results suggest that TSC-22 is a possible target of leukemia therapy.
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