ArticleNeurosurgery2012
WIP1 enhances tumor formation in a sonic hedgehog-dependent model of medulloblastoma.
Article in Neurosurgery, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Medulloblastoma and the DNA Damage Response.Frontiers in oncology · 2022Review
- Article
- High Expression ofCancers · 2021Article
- Modeling pediatric medulloblastoma.Brain pathology (Zurich, Switzerland) · 2020Review
- Non-canonical Hedgehog Signaling Pathway in Cancer: Activation of GLI Transcription Factors Beyond Smoothened.Frontiers in genetics · 2019Review
- The emerging roles of phosphatases in Hedgehog pathway.Cell communication and signaling : CCS · 2017Review
- WIP1 modulates responsiveness to Sonic Hedgehog signaling in neuronal precursor cells and medulloblastoma.Oncogene · 2016Article
- Evasion of cell senescence in SHH medulloblastoma.Cell cycle (Georgetown, Tex.) · 2016Review
- Wip1 phosphatase: between p53 and MAPK kinases pathways.Oncotarget · 2016Review
- Cooperative integration between HEDGEHOG-GLI signalling and other oncogenic pathways: implications for cancer therapy.Expert reviews in molecular medicine · 2015Review
- Knockdown of Wip1 Enhances Sensitivity to Radiation in HeLa Cells Through Activation of p38 MAPK.Oncology research · 2014Article
- The rationale for targeted therapies in medulloblastoma.Neuro-oncology · 2014Review
- Article
- Medulloblastomics: the end of the beginning.Nature reviews. Cancer · 2012Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundA significant number of medulloblastomas (MBs) originate from abnormal activation of the sonic hedgehog/patched (SHH/PTC) signaling pathway. Although p53 deficiency enhances tumor formation in mice, inactivation of the p53 gene is seen in a minority of MBs. Wild-type p53-induced phosphatase 1 (WIP1) downregulates p53 expression and has been shown to be overexpressed in MBs.
objectiveWe tested the hypothesis that overexpression of WIP1 enhances tumor formation in an SHH-dependent model of MB.
methodsWe used the RCAS/Ntv-a system to study the effect of WIP1 in vitro and in vivo. We transfected A375-TVA cells with RCAS-WIP1 and then exposed these cells to cisplatin to determine the effect on p53 expression. We modeled ectopic WIP1 expression independently and in combination with SHH in the cerebella of newborn mice to assess the effect on tumor formation. Mice were observed for 12 weeks or until neurological symptoms developed. The brains were examined for tumor formation.
resultsA375-TVA cells infected with RCAS-WIP1 demonstrated reduced p53 expression after exposure to cisplatin compared with controls. We detected tumors in 12 of 35 mice (34%) injected with RCAS-WIP1 and RCAS-SHH. Tumors were detected in 3 of 40 mice (8%) injected with RCAS-SHH alone. The difference in tumor formation rates was significant (χ(2) test, P = < .01). Tumors did not form in mice injected with RCAS-WIP1 alone.
conclusionWe show that ectopic expression of WIP1 cooperates with SHH to enhance formation of MB, although it is insufficient to induce tumors independently. Our results verify the role of WIP1 in MB formation and provide a crucial link to the inactivation of p53 in MBs.
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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.