ArticleOncogene2010
NF2-deficient cells depend on the Rac1-canonical Wnt signaling pathway to promote the loss of contact inhibition of proliferation.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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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.
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Who cites it
40 citing papers in PubMed, 61 citations in OpenAlex.
- The Wnt signaling networks in higher-grade meningiomas: from molecular pathogenesis to therapeutic innovation.Cancer cell international · 2026Review
- Identification of PKN2 and MOB4 as Coordinators of Collective Cell Migration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Gallbladder Schwannoma: A Case Report and Literature Review.Diagnostics (Basel, Switzerland) · 2025Article
- Morphological control of merlin-Rac antagonism in proliferation-promoting signaling.Science signaling · 2025Article
- Current molecular understanding of central nervous system schwannomas.Acta neuropathologica communications · 2025Review
- The molecular biology of NF2/Merlin on tumorigenesis and development.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Review
- Mechanisms of Cell Fusion in Cancer.Results and problems in cell differentiation · 2024Review
- A patient-derived organoid-based study identified an ASO targeting SNORD14E for endometrial cancer through reducing aberrant FOXM1 Expression and β-catenin nuclear accumulation.Journal of experimental & clinical cancer research : CR · 2023Article
- Article
- The genetic landscape and possible therapeutics of neurofibromatosis type 2.Cancer cell international · 2023Review
- Celastrol suppresses the growth of vestibular schwannoma in mice by promoting the degradation of β-catenin.Acta pharmacologica Sinica · 2022Article
- Identification of potent and novel inhibitors against RAC1: a Rho family GTPase.In silico pharmacology · 2022Article
- USP28 facilitates pancreatic cancer progression through activation of Wnt/β-catenin pathway via stabilising FOXM1.Cell death & disease · 2021Article
- The biological underpinnings of radiation therapy for vestibular schwannomas: Review of the literature.Laryngoscope investigative otolaryngology · 2021Review
- Identification and Validation of DEPDC1B as an Independent Early Diagnostic and Prognostic Biomarker in Liver Hepatocellular Carcinoma.Frontiers in genetics · 2021Article
- Merlin regulates signaling events at the nexus of development and cancer.Cell communication and signaling : CCS · 2020Review
- RAC1 Takes the Lead in Solid Tumors.Cells · 2019Review
- Cancer driver mutations in endometriosis: Variations on the major theme of fibrogenesis.Reproductive medicine and biology · 2018Review
- NF2/Merlin Inactivation and Potential Therapeutic Targets in Mesothelioma.International journal of molecular sciences · 2018Review
- Merlin inhibits Wnt/β-catenin signaling by blocking LRP6 phosphorylation.Cell death and differentiation · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The neurofibromatosis type 2 (NF2) tumor suppressor gene encodes merlin, a membrane/cytoskeleton protein necessary for the maintenance of contact inhibition of growth in cells. Bi-allelic inactivation of NF2 is known to cause multiple cancers in both humans and mice. However, the mechanism through which merlin exerts its tumor-suppressive function remains obscure. In this report, we show that NF2 knockout mouse embryonic fibroblasts lost contact inhibition of cell proliferation and contained significantly increased canonical Wnt signaling. Inhibition of Rac1, the activity of which is inversely regulated by NF2, through the use of a dominant-negative mutant, small hairpin RNA or a small molecule inhibitor in NF2-deficient cells, was able to suppress elevated Wnt signals as shown by reduced activity of the T-cell factor 4 (TCF4) transcription factor. Dominant-negative TCF4 or Rac1 mutant, as well as a small molecule inhibition of Wnt, were able to curb NF2 deficiency-elicited cell proliferation at the confluent state. Thus, Rac1-mediated canonical Wnt signaling is essential for the loss of contact inhibition in NF2-deficient cells.
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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.