ArticleLeukemia2004
Constitutive NF-kappaB DNA-binding activity in AML is frequently mediated by a Ras/PI3-K/PKB-dependent pathway.
Article in Leukemia, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 151 citations in OpenAlex.
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- Molecular Classification and Overcoming Therapy Resistance for Acute Myeloid Leukemia with Adverse Genetic Factors.International journal of molecular sciences · 2022Review
- Lower RNA expression of ALDH1A1 distinguishes the favorable risk group in acute myeloid leukemia.Molecular biology reports · 2022Review
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- Inflammatory Pathophysiology as a Contributor to Myeloproliferative Neoplasms.Frontiers in immunology · 2021Review
- Targeting PI3K/Akt/mTOR in AML: Rationale and Clinical Evidence.Journal of clinical medicine · 2020Review
- Article
- Aberrant GSK3β nuclear localization promotes AML growth and drug resistance.Blood advances · 2018Article
- NF-κB promotes the stem-like properties of leukemia cells by activation of LIN28B.World journal of stem cells · 2018Article
- MicroRNA-22 Suppresses Breast Cancer Cell Growth and Increases Paclitaxel Sensitivity by Targeting NRAS.Technology in cancer research & treatment · 2018Article
- Virosecurinine induces apoptosis in human leukemia THP-1 cells and other underlying molecular mechanisms.Oncology letters · 2018Article
- MicroRNA-29a Functions as a Tumor Suppressor and Increases Cisplatin Sensitivity by Targeting NRAS in Lung Cancer.Technology in cancer research & treatment · 2018Article
- CITED2 affects leukemic cell survival by interfering with p53 activation.Cell death & disease · 2017Article
- Targeting acute myeloid leukemia stem cell signaling by natural products.Molecular cancer · 2017Review
- MicroRNA-1301 inhibits proliferation of human glioma cells by directly targeting N-Ras.American journal of cancer research · 2017Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the present study, we aimed to elucidate the mechanism responsible for constitutive NF-kappaB DNA-binding activity in AML cells. Intervening in aberrant signaling pathway provides a rational approach for in vivo targeting of AML cells. Constitutive NF-kappaB DNA-binding activity was observed in 16 of 22 (73%) investigated AML cases and was, in general, associated with resistance to spontaneous apoptosis. Indeed, inhibition of NF-kappaB activity by the NF-kappaB inhibitor SN-50 peptide resulted in enhanced chemotherapy-induced apoptosis. In the majority of cases, constitutive NF-kappaB activity was mediated by a Ras/PI3 kinase (PI3-K)/protein kinase B (PKB)-mediated pathway. The PI3-K inhibitor Ly294002 and the Ras inhibitor L-744832 both inhibited PKB phosphorylation and NF-kappaB DNA-binding activity. The constitutive activation of Ras GTP-ase was caused by mutations in the gene encoding for N-Ras in 29% of the cases. The constitutive NF-kappaB activity could so far not be ascribed to the autocrine production of growth factors or to mutations in the Flt3 receptor, since anti-GM-CSF, -IL-1, -IL6, -TNFalpha or the tyrosine kinase inhibitor AG1296 did not affect the NF-kappaB DNA-binding activity. The present study demonstrates that Ras activation is an important pathway for triggering the NF-kappaB pathway in AML cells.
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