ArticleOncogene2003
Role for RhoB and PRK in the suppression of epithelial cell transformation by farnesyltransferase inhibitors.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
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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
19 citing papers in PubMed, 39 citations in OpenAlex.
- Zoledronic Acid Targeting of the Mevalonate Pathway Causes Reduced Cell Recruitment and Attenuates Pulmonary Fibrosis.Frontiers in pharmacology · 2022Article
- Transfer Learning via Deep Neural Networks for Implant Fixture System Classification Using Periapical Radiographs.Journal of clinical medicine · 2020Article
- Increased flux through the mevalonate pathway mediates fibrotic repair without injury.The Journal of clinical investigation · 2019Article
- Macrophage Rac2 Is Required to Reduce the Severity of Cigarette Smoke-induced Pneumonia.American journal of respiratory and critical care medicine · 2018Article
- Article
- Antimetabolite TTL-315 selectively kills glucose-deprived cancer cells and enhances responses to cytotoxic chemotherapy in preclinical models of cancer.Oncotarget · 2016Article
- Protein prenylation: unique fats make their mark on biology.Nature reviews. Molecular cell biology · 2016Review
- Targeting the isoprenoid pathway to abrogate progression of pulmonary fibrosis.Free radical biology & medicine · 2015Article
- Modulation of the mevalonate pathway by akt regulates macrophage survival and development of pulmonary fibrosis.The Journal of biological chemistry · 2014Article
- Rho isoform-specific interaction with IQGAP1 promotes breast cancer cell proliferation and migration.The Journal of biological chemistry · 2012Article
- Role of RhoB in the regulation of pulmonary endothelial and smooth muscle cell responses to hypoxia.Circulation research · 2012Article
- RhoB controls endothelial cell morphogenesis in part via negative regulation of RhoA.Vascular cell · 2012Article
- Mitochondrial Rac1 GTPase import and electron transfer from cytochrome c are required for pulmonary fibrosis.The Journal of biological chemistry · 2012Article
- Altered apoptotic responses in neurons lacking RhoB GTPase.The European journal of neuroscience · 2011Article
- Development of an intracellularly acting inhibitory peptide selective for PKN.The Biochemical journal · 2009Article
- Gene expression analysis of biological systems driving an organotypic model of endometrial carcinogenesis and chemoprevention.Gene regulation and systems biology · 2008Article
- RhoB regulates PDGFR-beta trafficking and signaling in vascular smooth muscle cells.Arteriosclerosis, thrombosis, and vascular biology · 2007Article
- RhoB facilitates c-Myc turnover by supporting efficient nuclear accumulation of GSK-3.Oncogene · 2006Article
- RhoB controls Akt trafficking and stage-specific survival of endothelial cells during vascular development.Genes & development · 2003Article
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 3 institutions in 1 country.
Funding
Abstract
Recent genetic investigations have established that RhoB gain-of-function is sufficient to mediate the antitransforming effects of farnesyltransferase inhibitors (FTIs) in H-Ras-transformed fibroblast systems. In this study, we addressed the breadth and mechanism of RhoB action in epithelial cells transformed by oncoproteins which are themselves insensitive to FTI inactivation. Rat intestinal epithelial (RIE) cells transformed by activated K-Ras or Rac1 were highly sensitive to FTI-induced actin reorganization and growth inhibition, despite the inability of FTI to block prenylation of either K-Ras or Rac1. Ectopic expression of the geranylgeranylated RhoB isoform elicited in cells by FTI treatment phenocopied these effects. Analysis of RhoB effector domain mutants pointed to a role for PRK, a Rho effector kinase implicated in the physiological function of RhoB in intracellular receptor trafficking, and these findings were supported further by experiments in a fibroblast system. We propose that FTIs recruit the antioncogenic RhoB protein in the guise of RhoB-GG to interfere with signaling by pro-oncogenic Rho proteins, possibly by sequestering common exchange factors or effectors such as PRK that are important for cell transformation.
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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.