ArticleOncogene2007
Transcriptomal profiling of the cellular transformation induced by Rho subfamily GTPases.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- SMARCA4 Inhibits Breast Cancer Progression and Metastasis through RHOA Suppression.Cancer research · 2025Article
- Screening of hub genes for sepsis-induced myopathy by weighted gene co-expression network analysis and protein-protein interaction network construction.BMC musculoskeletal disorders · 2024Article
- Force-mediated recruitment and reprogramming of healthy endothelial cells drive vascular lesion growth.Nature communications · 2024Article
- Investigation of the impact of bromodomain inhibition on cytoskeleton stability and contraction.Cell communication and signaling : CCS · 2024Article
- Investigation of the impact of bromodomain inhibition on cytoskeleton stability and contraction.bioRxiv : the preprint server for biology · 2023Article
- Mechanistic Interrogation of Cell Transformation In Vitro: The Transformics Assay as an Exemplar of Oncotransformation.International journal of molecular sciences · 2022Article
- Article
- p190 RhoGAP promotes contact inhibition in epithelial cells by repressing YAP activity.The Journal of cell biology · 2018Article
- Retinoid X Receptor Activation Alters the Chromatin Landscape To Commit Mesenchymal Stem Cells to the Adipose Lineage.Endocrinology · 2017Article
- C3 exoenzyme impairs cell proliferation and apoptosis by altering the activity of transcription factors.Naunyn-Schmiedeberg's archives of pharmacology · 2016Article
- Cooperative antiproliferative effect of coordinated ectopic expression of DLC1 tumor suppressor protein and silencing of MYC oncogene expression in liver cancer cells: Therapeutic implications.Oncology letters · 2016Article
- Small-Molecule Inhibition of Rho/MKL/SRF Transcription in Prostate Cancer Cells: Modulation of Cell Cycle, ER Stress, and Metastasis Gene Networks.Microarrays (Basel, Switzerland) · 2016Article
- OTUB1 de-ubiquitinating enzyme promotes prostate cancer cell invasion in vitro and tumorigenesis in vivo.Molecular cancer · 2015Article
- PIWIL2 induces c-Myc expression by interacting with NME2 and regulates c-Myc-mediated tumor cell proliferation.Oncotarget · 2014Article
- The Rho exchange factors Vav2 and Vav3 favor skin tumor initiation and promotion by engaging extracellular signaling loops.PLoS biology · 2013Article
- Article
- Expression of VAV1 in the tumour microenvironment of glioblastoma multiforme.Journal of neuro-oncology · 2012Article
- Chd2 interacts with H3.3 to determine myogenic cell fate.The EMBO journal · 2012Article
- MicroRNA-34a suppresses malignant transformation by targeting c-Myc transcriptional complexes in human renal cell carcinoma.Carcinogenesis · 2012Article
- RhoGDIα-dependent balance between RhoA and RhoC is a key regulator of cancer cell tumorigenesis.Molecular biology of the cell · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
We have used microarray technology to identify the transcriptional targets of Rho subfamily guanosine 5'-triphosphate (GTP)ases in NIH3T3 cells. This analysis indicated that murine fibroblasts transformed by these proteins show similar transcriptomal profiles. Functional annotation of the regulated genes indicate that Rho subfamily GTPases target a wide spectrum of functions, although loci encoding proteins linked to proliferation and DNA synthesis/transcription are upregulated preferentially. Rho proteins promote four main networks of interacting proteins nucleated around E2F, c-Jun, c-Myc and p53. Of those, E2F, c-Jun and c-Myc are essential for the maintenance of cell transformation. Inhibition of Rock, one of the main Rho GTPase targets, leads to small changes in the transcriptome of Rho-transformed cells. Rock inhibition decreases c-myc gene expression without affecting the E2F and c-Jun pathways. Loss-of-function studies demonstrate that c-Myc is important for the blockage of cell-contact inhibition rather than for promoting the proliferation of Rho-transformed cells. However, c-Myc overexpression does not bypass the inhibition of cell transformation induced by Rock blockage, indicating that c-Myc is essential, but not sufficient, for Rock-dependent transformation. These results reveal the complexity of the genetic program orchestrated by the Rho subfamily and pinpoint protein networks that mediate different aspects of the malignant phenotype of Rho-transformed cells.
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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.