ReviewCell death & disease2019
The impact of oncogenic RAS on redox balance and implications for cancer development.
Review in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 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.
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.
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Who cites it
63 citing papers in PubMed, 98 citations in OpenAlex.
- Herbal and functional food phytochemicals in chronic disease: modulating oxidative stress and health outcomes.Molecular biology reports · 2026Review
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- Lipid remodeling and ferroptosis in phosphatidylcholine-mediated tumor-stroma crosstalk.Frontiers in molecular biosciences · 2026Review
- Review
- Preparation and Characterization of Novel Pan-RAS Inhibitor Loaded Ultraflexible Liposomes for the Topical Prevention or Treatment of Skin Melanoma.Pharmaceutical research · 2025Article
- Metabolic Regulation of Ferroptosis in Breast Cancer.International journal of molecular sciences · 2025Review
- Article
- Nanomedicine-Driven Modulation of Reductive Stress for Cancer Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- The complex journey of targeting RAS in oncology.BMC cancer · 2025Review
- Cytoplasmic Vacuolization: A Fascinating Morphological Alteration From Cellular Stress to Cell Death.Cancer science · 2025Review
- Ellipticine targets FGFR3 to mediate the RAS/MAPK-P38 signalling pathway to induce apoptosis in hepatocellular carcinoma cells.3 Biotech · 2025Article
- Mechanisms of HRAS regulation of liver hepatocellular carcinoma for prognosis prediction.BMC cancer · 2025Article
- The Role of Reactive Oxygen Species in Colorectal Cancer Initiation and Progression: Perspectives on Theranostic Approaches.Cancers · 2025Review
- Anticancer Activity of Imidazolyl Gold(I/III) Compounds in Non-Small Cell Lung Cancer Cell Lines.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Article
- Combinatorial strategies to target RAS-driven cancers.Nature reviews. Cancer · 2024Review
- Pan-cancer evaluation of regulated cell death to predict overall survival and immune checkpoint inhibitor response.NPJ precision oncology · 2024Article
- Silver Nanoparticles Selectively Treat Neurofibromatosis Type 1-Associated Plexiform Neurofibroma Cells at Doses That Do Not Affect Patient-Matched Schwann Cells.Pharmaceutics · 2024Article
- Targeting ROS production through inhibition of NADPH oxidases.Nature chemical biology · 2023Article
- The Cardiofaciocutaneous Syndrome: From Genetics to Prognostic-Therapeutic Implications.Genes · 2023Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The RAS family of proto-oncogenes comprises HRAS, KRAS, and NRAS, which are among the most mutated genes in human cancers. The RAS family genes encode small GTPases that coordinate key signaling pathways in response to growth factors. Mutations in RAS result in a constitutively active form of the protein that supports cellular transformation and tumorigenesis. The mechanisms of oncogenic RAS-mediated transformation encompass uncontrolled proliferation and inhibition of cell death through overactivation of the RAF-MEK-ERK and the PI3K-AKT pathways, respectively. In addition, the control of redox balance by RAS has also been proposed to play a role in its oncogenic properties. However, the exact role of redox balance in mediating mutant RAS transformation is still under debate. Here, we present, on one hand, the involvement of pro-oxidant components in oncogenic RAS transformation, such as NADPH oxidases and mitochondrial reactive oxygen species, and how these promote transformation. On the other hand, we describe the contribution of antioxidant components to mutant RAS transformation, including Nrf2, glutathione biosynthesis and xCT, as well as the mechanisms by which antioxidant programs drive transformation. Finally, we aim to reconcile the seemingly opposite effects of oncogenic RAS on redox balance and discuss a model for the complementary role of both pro-oxidant and antioxidant pathways in mutant RAS-driven tumor progression.
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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.