ReviewOncogene2017
Rho GTPases: Anti- or pro-neoplastic targets?
Review in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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
58 citing papers in PubMed, 101 citations in OpenAlex.
- Implications of Rho GTPase signaling in cancer immunotherapy.Biochemical Society transactions · 2026Review
- ARHGAP44 gene: a cytoskeleton mobility-related modulator with implications in pan-cancer prognostic risk and immune regulation.Frontiers in oncology · 2026Article
- Advances in Understanding How RhoB Regulates Akt Inhibition Efficacy in NSCLC.Current cancer drug targets · 2026Article
- TMEM121 suppresses cervical cancer cell proliferation and migration via interaction with the ERK pathway.American journal of cancer research · 2026Article
- Rac1 in gastric cancer: a molecular driver of invasion, EMT, and therapeutic resistance.Journal of translational medicine · 2025Review
- Pan-cancer analyses identify oncogenic drivers, expression signatures, and therapeutic vulnerabilities in RHO GTPase pathway genes.Frontiers in bioinformatics · 2025Article
- Tumor-derived RHOA mutants interact with effectors in the GDP-bound state.Nature communications · 2024Article
- FOXA2 Activates RND1 to Regulate Arachidonic Acid Metabolism Pathway and Suppress Cisplatin Resistance in Lung Squamous Cell Carcinoma.The clinical respiratory journal · 2024Article
- Structural basis for the distinct roles of non-conserved Pro116 and conserved Tyr124 of BCH domain of yeast p50RhoGAP.Cellular and molecular life sciences : CMLS · 2024Article
- Circulating miRNAs and Preeclampsia: From Implantation to Epigenetics.International journal of molecular sciences · 2024Review
- ARHGEF16 expression correlates with proliferation, migration and invasion of colon cancer cells.Translational cancer research · 2023Article
- Role of Rho GTPases in inflammatory bowel disease.Cell death discovery · 2023Review
- Fixing the GAP: The role of RhoGAPs in cancer.European journal of cell biology · 2022Review
- Aberrant Expression and Subcellular Localization of ECT2 Drives Colorectal Cancer Progression and Growth.Cancer research · 2022Article
- The role of GTPase-activating protein ARHGAP26 in human cancers.Molecular and cellular biochemistry · 2022Review
- Group I p21-activated kinases in leukemia cell adhesion to fibronectin.Cell adhesion & migration · 2021Article
- Multi-omic profiling of peritoneal metastases in gastric cancer identifies molecular subtypes and therapeutic vulnerabilities.Nature cancer · 2021Article
- Structural basis for p50RhoGAP BCH domain-mediated regulation of Rho inactivation.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Recombinant anthrax lethal toxin inhibits cell motility and invasion in breast cancer cells through the dysregulation of Rho GTPases.Oncology letters · 2021Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Rho GTPases are critical signal transducers of multiple pathways. They have been proposed to be useful anti-neoplastic targets for over two decades, especially in Ras-driven cancers. Until recently, however, few in vivo studies had been carried out to test this premise. Several recent mouse model studies have verified that Rac1, RhoA, and some of their effector proteins such as PAK and ROCK, are likely anti-cancer targets for treating K-Ras-driven tumours. Other seemingly contradictory studies have suggested that at least in certain instances inhibition of individual Rho GTPases may paradoxically result in pro-neoplastic effects. Significantly, both RhoA GTPase gain- and loss-of-function mutations have been discovered in primary leukemia/lymphoma and gastric cancer by human cancer genome sequencing efforts, suggesting both pro- and anti-neoplastic roles. In this review we summarize and integrate these unexpected findings and discuss the mechanistic implications in the design and application of Rho GTPase targeting strategies in future cancer therapies.
Indexed as
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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.