ArticleMolecular and cellular biology1995
Evidence that farnesyltransferase inhibitors suppress Ras transformation by interfering with Rho activity.
Article in Molecular and cellular biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 222 citations in OpenAlex.
- Uncovering protein prenylation in Th1 cells: novel prenylation sites and insights into statin and farnesyltransferase inhibition.BMC biology · 2025Article
- Article
- BAG6 supports stress fiber formation by preventing the ubiquitin-mediated degradation of RhoA.Molecular biology of the cell · 2023Article
- Potential of Farnesyl Transferase Inhibitors in Combination Regimens in Squamous Cell Carcinomas.Cancers · 2021Article
- Overexpression of FNTB and the activation of Ras induce hypertrophy and promote apoptosis and autophagic cell death in cardiomyocytes.Journal of cellular and molecular medicine · 2020Article
- Targeted Quantitative Proteomics Revealed Arsenite-induced Proteasomal Degradation of RhoB in Fibroblast Cells.Chemical research in toxicology · 2019Article
- The Cullin-3-Rbx1-KCTD10 complex controls endothelial barrier function via K63 ubiquitination of RhoB.The Journal of cell biology · 2018Article
- RhoB: Team Oncogene or Team Tumor Suppressor?Genes · 2018Review
- Variability in statin-induced changes in gene expression profiles of pancreatic cancer.Scientific reports · 2017Article
- Critical functions of RhoB in support of glioblastoma tumorigenesis.Neuro-oncology · 2015Article
- RhoB modifies estrogen responses in breast cancer cells by influencing expression of the estrogen receptor.Breast cancer research : BCR · 2013Article
- A multiplicity of anti-invasive effects of farnesyl transferase inhibitor SCH66336 in human head and neck cancer.International journal of cancer · 2012Article
- RhoB links PDGF signaling to cell migration by coordinating activation and localization of Cdc42 and Rac.Journal of cellular biochemistry · 2011Article
- Breast cancer stem cells survive periods of farnesyl-transferase inhibitor-induced dormancy by undergoing autophagy.Bone marrow research · 2011Article
- Epigenetic regulation of RhoB loss of expression in lung cancer.BMC cancer · 2007Article
- Farnesyltransferase inhibitors inhibit T-cell cytokine production at the posttranscriptional level.Blood · 2007Article
- GTP-binding proteins of the Rho/Rac family: regulation, effectors and functions in vivo.BioEssays : news and reviews in molecular, cellular and developmental biology · 2007Review
- EGFR, ErbB2 and Ras but not Src suppress RhoB expression while ectopic expression of RhoB antagonizes oncogene-mediated transformation.Oncogene · 2004Article
- RhoB controls Akt trafficking and stage-specific survival of endothelial cells during vascular development.Genes & development · 2003Article
- Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Small-molecule inhibitors of the housekeeping enzyme farnesyltransferase (FT) suppress the malignant growth of Ras-transformed cells. Previous work suggested that the activity of these compounds reflected effects on actin stress fiber regulation rather than Ras inhibition. Rho proteins regulate stress fiber formation, and one member of this family, RhoB, is farnesylated in vivo. Therefore, we tested the hypothesis that interference with RhoB was the principal basis by which the peptidomimetic FT inhibitor L-739,749 suppressed Ras transformation. The half-life of RhoB was found to be approximately 2 h, supporting the possibility that it could be functionally depleted within the 18-h period required by L-739,749 to induce reversion. Cell treatment with L-739,749 disrupted the vesicular localization of RhoB but did not effect the localization of the closely related RhoA protein. Ras-transformed Rat1 cells ectopically expressing N-myristylated forms of RhoB (Myr-rhoB), whose vesicular localization was unaffected by L-739,749, were resistant to drug treatment. The protective effect of Myr-rhoB required the integrity of the RhoB effector domain and was not due to a gain-of-function effect of myristylation on cell growth. In contrast, Rat1 cells transformed by a myristylated Ras construct remained susceptible to growth inhibition by L-739,749. We concluded that Rho is necessary for Ras transformation and that FT inhibitors suppress the transformed phenotype at least in part by direct or indirect interference with Rho, possibly with RhoB itself.
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