ArticleCancer biology & therapy2007
Raf inhibitor stabilizes receptor for the type I interferon but inhibits its anti-proliferative effects in human malignant melanoma cells.
Article in Cancer biology & therapy, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Interferon alpha for the adjuvant treatment of cutaneous melanoma.The Cochrane database of systematic reviews · 2013Pooled it
- Molecular characteristics and therapeutic implications of Toll-like receptor signaling pathway in melanoma.Scientific reports · 2023Article
- Linoleate-pazopanib conjugation as active pharmacological ingredient to abolish hepatocellular carcinoma growth.Frontiers in pharmacology · 2023Article
- Malignant cell-specific pro-tumorigenic role of type I interferon receptor in breast cancers.Cancer biology & therapy · 2020Article
- A PotentClinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
- Suppression of Type I Interferon Signaling Overcomes Oncogene-Induced Senescence and Mediates Melanoma Development and Progression.Cell reports · 2016Article
- Combining immunotherapy with oncogene-targeted therapy: a new road for melanoma treatment.Frontiers in immunology · 2015Review
- Interferons and their stimulated genes in the tumor microenvironment.Seminars in oncology · 2014Review
- Future perspectives in melanoma research. Meeting report from the "Melanoma Bridge. Napoli, December 2nd-4th 2012".Journal of translational medicine · 2013Article
- Hope and fear for interferon: the receptor-centric outlook on the future of interferon therapy.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2013Review
- Activation of the Ras/Raf/MEK pathway facilitates hepatitis C virus replication via attenuation of the interferon-JAK-STAT pathway.Journal of virology · 2012Article
- Article
- Melanoma cell-secreted soluble factor that stimulates ubiquitination and degradation of the interferon alpha receptor and attenuates its signaling.Pigment cell & melanoma research · 2010Article
- Ubiquitination-dependent regulation of signaling receptors in cancer.Genes & cancer · 2010Article
- Virus-induced unfolded protein response attenuates antiviral defenses via phosphorylation-dependent degradation of the type I interferon receptor.Cell host & microbe · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Interferon alpha (IFNalpha) is widely used in treatment of malignant melanoma patients. This cytokine acts on cells by engaging Type I IFN receptor consisting of two subunits, (IFNAR1 and IFNAR2) followed by activation of Janus kinases (Jak). Levels of IFNAR1 (regulated via degradation mediated by the betaTrcp E3 ubiquitin ligase) and IFNalpha signaling were reduced in 1205Lu melanoma cell line that harbors activated BRAF and exhibits high levels of betaTrcp ubiquitin ligase. Expression of stabilized IFNAR1 in melanoma cells decreased their tumorigenicity. Furthermore, RNAi-mediated BRAF knockdown and pharmacologic inhibition of either Raf or MEK1 decreased levels of betaTrcp and stabilized IFNAR1. However, despite causing stabilization of IFNAR1, Raf inhibitor BAY 43-9006 interfered with cellular responses to IFNalpha most likely due to its ability to directly inhibit Jak activity. We discuss the implications of this result for combination therapy with BAY 43-9006 and IFNalpha in melanoma patients.
Indexed as
Identifiers
What OpenQuestion holds
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.