ArticleMolecular cancer research : MCR2008
WT1 induction of mitogen-activated protein kinase phosphatase 3 represents a novel mechanism of growth suppression.
Article in Molecular cancer research : MCR, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 18 citations in OpenAlex.
- WT1 gene: a potential therapeutic target for multiple cancer treatment strategies.Clinical and experimental medicine · 2025Review
- A systematic analysis of genetic interactions and their underlying biology in childhood cancer.Communications biology · 2021Article
- Wilms' tumor 1 (Cell cycle (Georgetown, Tex.) · 2020Article
- Dysregulation of Dual-Specificity Phosphatases by Epstein-Barr Virus LMP1 and Its Impact on Lymphoblastoid Cell Line Survival.Journal of virology · 2020Article
- Classification of a frameshift/extended and a stop mutation in WT1 as gain-of-function mutations that activate cell cycle genes and promote Wilms tumour cell proliferation.Human molecular genetics · 2014Article
- Mechanisms of transcriptional regulation by WT1 (Wilms' tumour 1).The Biochemical journal · 2014Review
- SIRT1 promotes N-Myc oncogenesis through a positive feedback loop involving the effects of MKP3 and ERK on N-Myc protein stability.PLoS genetics · 2011Article
- Functional characterization of Wilms tumor-suppressor WTX and tumor-associated mutants.Oncogene · 2011Article
- DUSP1/MKP1 promotes angiogenesis, invasion and metastasis in non-small-cell lung cancer.Oncogene · 2011Article
- Wilms' tumours: about tumour suppressor genes, an oncogene and a chameleon gene.Nature reviews. Cancer · 2011Review
- Wilms tumor 1 (WT1) regulates KRAS-driven oncogenesis and senescence in mouse and human models.The Journal of clinical investigation · 2010Article
- An integrated genome screen identifies the Wnt signaling pathway as a major target of WT1.Proceedings of the National Academy of Sciences of the United States of America · 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
4 authors at 3 institutions in 1 country.
Funding
Abstract
In its role as a tumor suppressor, WT1 transactivates several genes that are regulators of cell growth and differentiation pathways. For instance, WT1 induces the expression of the cell cycle regulator p21, the growth-regulating glycoprotein amphiregulin, the proapoptotic gene Bak, and the Ras/mitogen-activated protein kinase (MAPK) inhibitor Sprouty1. Here, we show that WT1 transactivates another important negative regulator of the Ras/MAPK pathway, MAPK phosphatase 3 (MKP3). In a WT1-inducible cell line that exhibits decreased cell growth and increased apoptosis on expression of WT1, microarray analysis showed that MKP3 is the most highly induced gene. This was confirmed by real-time PCR where MKP3 and other members of the fibroblast growth factor 8 syn expression group, which includes Sprouty 1 and the Ets family of transcription factors, were induced rapidly following WT1 expression. WT1 induction was associated with a block in the phosphorylation of extracellular signal-regulated kinase in response to epidermal growth factor stimulation, an effect mediated by MKP3. In the presence of a dominant-negative MKP3, WT1 could no longer block phosphorylation of extracellular signal-regulated kinase. Lastly, when MKP3 expression is down-regulated by short hairpin RNA, WT1 is less able to block Ras-mediated transformation of 3T3 cells.
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.