ArticleThe Journal of biological chemistry2004
Arsenite sensitizes human melanomas to apoptosis via tumor necrosis factor alpha-mediated pathway.
Article in The Journal of biological chemistry, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 58 citations in OpenAlex.
- Hepatocyte TIA1 constrains metabolic steatohepatitis by translationally suppressing Srebf1 mRNA in stress granules.Cell death & disease · 2026Article
- The synergistic inhibitory effect of combining therapies targeting EGFR and mitochondria in sarcomas.Oncotarget · 2020Article
- 2,3,5,6-Tetramethylpyrazine (TMP) down-regulated arsenic-induced heme oxygenase-1 and ARS2 expression by inhibiting Nrf2, NF-κB, AP-1 and MAPK pathways in human proximal tubular cells.Archives of toxicology · 2016Article
- Regulation of viability, differentiation and death of human melanoma cells carrying neural stem cell biomarkers: a possibility for neural trans-differentiation.Apoptosis : an international journal on programmed cell death · 2015Article
- Tetramethylpyrazine (TMP) protects against sodium arsenite-induced nephrotoxicity by suppressing ROS production, mitochondrial dysfunction, pro-inflammatory signaling pathways and programed cell death.Archives of toxicology · 2015Article
- Melanocytes and keratinocytes have distinct and shared responses to ultraviolet radiation and arsenic.Toxicology letters · 2014Article
- Sodium arsenite exposure inhibits AKT and Stat3 activation, suppresses self-renewal and induces apoptotic death of embryonic stem cells.Apoptosis : an international journal on programmed cell death · 2013Article
- Article
- Regulation of apoptosis in human melanoma and neuroblastoma cells by statins, sodium arsenite and TRAIL: a role of combined treatment versus monotherapy.Apoptosis : an international journal on programmed cell death · 2011Article
- Suppression of the proinflammatory response of metastatic melanoma cells increases TRAIL-induced apoptosis.Journal of cellular biochemistry · 2011Article
- Disruption of IGF-1R signaling increases TRAIL-induced apoptosis: a new potential therapy for the treatment of melanoma.Experimental cell research · 2010Article
- Arsenic trioxide and ascorbic acid demonstrate promising activity against primary human CLL cells in vitro.Leukemia research · 2010Article
- Radiation-induced bystander signaling pathways in human fibroblasts: a role for interleukin-33 in the signal transmission.Cellular signalling · 2010Article
- The PTEN-AKT3 signaling cascade as a therapeutic target in melanoma.Pigment cell & melanoma research · 2009Review
- Biological responses to arsenic compounds.The Journal of biological chemistry · 2009Review
- Inhibition of ataxia telangiectasia mutated kinase activity enhances TRAIL-mediated apoptosis in human melanoma cells.Cancer research · 2009Article
- Sensitivity to sodium arsenite in human melanoma cells depends upon susceptibility to arsenite-induced mitotic arrest.Toxicology and applied pharmacology · 2008Article
- Radiosensitization of melanoma cells through combined inhibition of protein regulators of cell survival.Apoptosis : an international journal on programmed cell death · 2008Article
- Resveratrol sensitizes melanomas to TRAIL through modulation of antiapoptotic gene expression.Experimental cell research · 2008Article
- Sequential treatment by ionizing radiation and sodium arsenite dramatically accelerates TRAIL-mediated apoptosis of human melanoma cells.Cancer research · 2007Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Arsenic is a well established human carcinogen and is associated with a variety of cancers including those of the skin. Paradoxically, arsenic has also been used, amid at low doses, in the treatment of leukemia for over a century. Here we demonstrate that low to moderate concentrations of arsenite (2-10 microm) that has little or no effect on normal melanocytes may induce apoptosis of human melanomas including highly metastatic ones despite their low surface Fas levels. The two prerequisites that dictate apoptotic response of melanomas upon arsenite treatment are low nuclear NF-kappaB activity and an endogenous expression of tumor necrosis factor alpha. Under these conditions, melanoma cells acquired sensitivity to tumor necrosis factor alpha-mediated killing. On the other hand, signaling pathways including those of phosphatidylinositol 3-kinase-AKT, MEK-ERK, and JNK play a protective role against arsenite-induced oxidative stress and apoptosis in melanoma cells. Suppression of these pathways dramatically accelerates arsenite-induced apoptosis. Taken together, these data could provide potential approaches to sensitize melanomas to the cytotoxic effects of arsenite through modulating the signaling pathways.
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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.