ArticleOncotarget2010
FLIP regulation of HO-1 and TNF signalling in human acute myeloid leukemia provides a unique secondary anti-apoptotic mechanism.
Article in Oncotarget, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Metabolic Signature ofJournal of personalized medicine · 2025Review
- The prognostic and therapeutic potential of HO-1 in leukemia and MDS.Cell communication and signaling : CCS · 2023Review
- Targeting the NRF2/HO-1 Antioxidant Pathway in FLT3-ITD-Positive AML Enhances Therapy Efficacy.Antioxidants (Basel, Switzerland) · 2022Article
- Novel Targeted Nano-Parthenolide Molecule against NF-kB in Acute Myeloid Leukemia.Molecules (Basel, Switzerland) · 2019Article
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- Aberrant nuclear factor-kappa B activity in acute myeloid leukemia: from molecular pathogenesis to therapeutic target.Oncotarget · 2015Review
- Ibrutinib inhibits SDF1/CXCR4 mediated migration in AML.Oncotarget · 2014Article
- Retinoic acid synergizes ATO-mediated cytotoxicity by precluding Nrf2 activity in AML cells.British journal of cancer · 2014Article
- CXXC5 (retinoid-inducible nuclear factor, RINF) is a potential therapeutic target in high-risk human acute myeloid leukemia.Oncotarget · 2013Article
- Attenuation of dexamethasone-induced cell death in multiple myeloma is mediated by miR-125b expression.Cell cycle (Georgetown, Tex.) · 2013Article
- Cellular FLICE-like inhibitory protein long form (c-FLIPL) overexpression is related to cervical cancer progression.International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists · 2013Article
- A combination of temsirolimus, an allosteric mTOR inhibitor, with clofarabine as a new therapeutic option for patients with acute myeloid leukemia.Oncotarget · 2012Article
- Bortezomib induces heme oxygenase-1 expression in multiple myeloma.Cell cycle (Georgetown, Tex.) · 2012Article
- The role of TRADD in death receptor signaling.Cell cycle (Georgetown, Tex.) · 2012Review
- Systemic use of tumor necrosis factor alpha as an anticancer agent.Oncotarget · 2011Review
- Pleiotropic functions of EAPII/TTRAP/TDP2: cancer development, chemoresistance and beyond.Cell cycle (Georgetown, Tex.) · 2011Review
- Linear polyubiquitin chains: a new modifier involved in NFκB activation and chronic inflammation, including dermatitis.Cell cycle (Georgetown, Tex.) · 2011Article
- Protection of acute myeloid leukaemia cells from apoptosis induced by front-line chemotherapeutics is mediated by haem oxygenase-1.Oncotarget · 2011Article
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5 authors at 2 institutions in 1 country.
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Abstract
Acute myeloid leukemia (AML) comprises a heterogeneous group of clonal disorders of hematopoietic progenitors. We previously showed that heme oxygenase-1 (HO-1/Hsp32) underlies resistance of AML to TNF-induced apoptosis. Here we show for the first time that the modulatory protein, FLICE-inhibitory protein (FLIP) indirectly regulates induction of HO-1 in response to TNF in human AML blasts, but not non-cancerous control cells. In AML cells, TNF-induced FLIP expression was an NF-κB-dependent event, and silencing of FLIP isoforms (FLIPL, FLIPS and FLIPR) induced pro-apoptotic responses to TNF, with FLIPL knock-down providing the greatest apoptotic switch. However, FLIPL knock-down consequently increased expression of HO-1; a response that occurred in AML (but not non-cancerous) cells to protect a proportion of them from apoptotic death. Our results show that increases in HO-1 induced an apoptotic-resistant form in AML cells in the absence of FLIPL. This is the first time that FLIPL has been shown to regulate the expression of HO-1. These data reveal unique regulatory networks in cancerous AML cells whereby FLIP regulation of HO-1 provides AML cells with secondary anti-apoptotic protection against extrinsic factors (eg TNF/chemotherapies) that try to switch on death signals in these highly death-resistant cells. Future AML therapies should target these mechanisms.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.