ArticleJournal of neuro-oncology2005
FAS associated phosphatase (FAP-1) blocks apoptosis of astrocytomas through dephosphorylation of FAS.
Article in Journal of neuro-oncology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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
21 citing papers in PubMed, 37 citations in OpenAlex.
- Arsenic disulfide promoted the demethylation ofPeerJ · 2024Article
- Role of Non-Receptor-Type Tyrosine Phosphatases in Brain-Related Diseases.Molecular neurobiology · 2023Review
- The dual role of the CD95 and CD95L signaling pathway in glioblastoma.Frontiers in immunology · 2022Review
- Dual Role of the PTPN13 Tyrosine Phosphatase in Cancer.Biomolecules · 2020Review
- Apoptotic signalling targets the post-endocytic sorting machinery of the death receptor Fas/CD95.Nature communications · 2019Article
- Protein tyrosine phosphatases: promising targets in pancreatic ductal adenocarcinoma.Cellular and molecular life sciences : CMLS · 2019Review
- Review
- Protein Tyrosine Phosphatase-N13 Promotes Myofibroblast Resistance to Apoptosis in Idiopathic Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2018Article
- The impact of phosphatases on proliferative and survival signaling in cancer.Cellular and molecular life sciences : CMLS · 2018Review
- Sildenafil (Viagra) sensitizes prostate cancer cells to doxorubicin-mediated apoptosis through CD95.Oncotarget · 2016Article
- Heterogeneous glioblastoma cell cross-talk promotes phenotype alterations and enhanced drug resistance.Oncotarget · 2015Article
- Article
- Valosin containing protein (VCP/p97) is a novel substrate for the protein tyrosine phosphatase PTPL1.Experimental cell research · 2013Article
- PTPN13/PTPL1: an important regulator of tumor aggressiveness.Anti-cancer agents in medicinal chemistry · 2011Review
- miR-200c regulates induction of apoptosis through CD95 by targeting FAP-1.Molecular cell · 2010Article
- Protein tyrosine phosphatases in glioma biology.Acta neuropathologica · 2010Review
- Missense polymorphisms of PTPRJ and PTPN13 genes affect susceptibility to a variety of human cancers.Journal of cancer research and clinical oncology · 2010Article
- Genetic polymorphisms in the PTPN13 gene and risk of squamous cell carcinoma of head and neck.Carcinogenesis · 2009Article
- PTPL1: a large phosphatase with a split personality.Cancer metastasis reviews · 2008Review
- siRNA Down-regulation of the PATZ1 Gene in Human Glioma Cells Increases Their Sensitivity to Apoptotic Stimuli.Cancer therapy · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Astrocytomas are the most common primary tumor of the adult human central nervous system. Despite efforts to develop more effective clinical treatment strategies, median survival time for patients with the most severe form of astrocytoma, glioblastoma multiforme (GBM), remains about one year. Astrocytomas are resistant to cytotoxic therapy in general and radiation therapy in particular, greatly limiting treatment options. One reason for this seems to be defects in the pathways controlling apoptosis. We have characterized the role of the tyrosine phosphatase FAP-1 (FAS-associated phosphatase 1) in astrocytomas. Our studies demonstrate that FAP-1 is overexpressed in astrocytomas and this contributes to the resistance of the tumor cells to FAS-mediated apoptosis. We demonstrate that knockdown of FAP-1 by RNA interference leads to increased apoptosis and increased sensitivity of astrocytoma cells to FAS-induced cell death. FAP-1 binds to FAS in a ligand-dependent manner and forms a signaling complex that modulates the ability of astrocytoma cells to undergo FAS ligand (FASL)-mediated cell death. In astrocytoma cells, FASL treatment induces tyrosine phosphorylation of FAS. FAP-1 dephosphorylates phospho-tyrosine 275 in the carboxyl terminus of FAS. This is the first direct evidence that FAS activity can be regulated by reversible phosphorylation and suggests a mechanism for astrocytoma resistance to apoptosis.
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.