ArticleOncotarget2016
C3G knock-down enhances migration and invasion by increasing Rap1-mediated p38α activation, while it impairs tumor growth through p38α-independent mechanisms.
Article in Oncotarget, 2016. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- C3G Downregulation Enhances Stemness in Glioblastoma Cells by Promoting PKM2 Upregulation.International journal of biological sciences · 2026Article
- C3G deregulation uncovers a dual role in B-cell lymphoma: tumor suppression and enhanced metastasis via Rap1 and Rac2 signaling.Cell communication and signaling : CCS · 2025Article
- Deletion of C3G in hepatocytes impairs full liver maturation and alters glucose homeostasis.Cell death & disease · 2025Article
- Platelet C3G protects from liver fibrosis, while enhancing tumor growth through regulation of the immune response.The Journal of pathology · 2025Article
- New and Old Key Players in Liver Cancer.International journal of molecular sciences · 2023Review
- Talin‑1 interaction network in cellular mechanotransduction (Review).International journal of molecular medicine · 2022Review
- C3G down-regulation enhances pro-migratory and stemness properties of oval cells by promoting an epithelial-mesenchymal-like process.International journal of biological sciences · 2022Article
- C3G Protein, a New Player in Glioblastoma.International journal of molecular sciences · 2021Review
- Centrosome Dynamics and Its Role in Inflammatory Response and Metastatic Process.Biomolecules · 2021Review
- Article
- C3G downregulation induces the acquisition of a mesenchymal phenotype that enhances aggressiveness of glioblastoma cells.Cell death & disease · 2021Article
- Expression of a novel brain specific isoform of C3G is regulated during development.Scientific reports · 2020Article
- Large Extracellular Vesicle-Associated Rap1 Accumulates in Atherosclerotic Plaques, Correlates With Vascular Risks and Is Involved in Atherosclerosis.Circulation research · 2020Article
- C3G Is Upregulated in Hepatocarcinoma, Contributing to Tumor Growth and Progression and to HGF/MET Pathway Activation.Cancers · 2020Article
- C3G contributes to platelet activation and aggregation by regulating major signaling pathways.Signal transduction and targeted therapy · 2020Article
- Novel compound cedrelone inhibits hepatocellular carcinoma progression via PBLD and Ras/Rap1.Experimental and therapeutic medicine · 2019Article
- Inhibition of Epac2 Attenuates Neural Cell Apoptosis and Improves Neurological Deficits in a Rat Model of Traumatic Brain Injury.Frontiers in neuroscience · 2018Article
- How Rap and its GEFs control liver physiology and cancer development. C3G alterations in human hepatocarcinoma.Hepatic oncology · 2018Review
- C3G promotes a selective release of angiogenic factors from activated mouse platelets to regulate angiogenesis and tumor metastasis.Oncotarget · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
C3G, a Guanine nucleotide Exchange Factor (GEF) for Rap1 and R-Ras, has been shown to play important roles in development and cancer. Previous studies determined that C3G regulates cell death through down-regulation of p38α MAPK activity. Here, we found that C3G knock-down in MEFs and HCT116 cells promotes migration and invasion through Rap1-mediated p38α hyper-activation. These effects of C3G were inhibited by Rap1 knock-down or inactivation. The enhanced migration observed in C3G depleted HCT116 cells was associated with reduction in E-cadherin expression, internalization of ZO-1, actin cytoskeleton reorganization and decreased adhesion. We also found that matrix metalloproteases MMP2 and MMP9 are involved in the pro-invasive effect of C3G down-regulation. Additionally, our studies revealed that both C3G and p38α collaborate to promote growth of HCT116 cells in vitro and in vivo, possibly by enhancing cell survival. In fact, knocking-down C3G or p38α individually or together promoted cell death in vitro, although only the double C3G-p38α silencing was able to increase cell death within tumors. Notably, we found that the pro-tumorigenic function of C3G does not depend on p38α or Rap1 activation. Altogether, our studies uncover novel mechanisms by which C3G controls key aspects of tumorigenesis.
Indexed as
Identifiers
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.