ReviewCell communication and signaling : CCS2023
KRAS, MYC, and ARF6: inseparable relationships cooperatively promote cancer malignancy and immune evasion.
Review in Cell communication and signaling : CCS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 25 citations in OpenAlex.
- Multi-omics characterization of chronic social defeat stress recall-activated nuclei in Arc-GFP mice.Molecular psychiatry · 2026Article
- Targeting ARF6-SUCNR1 Axis: Antisense Oligonucleotide Adjuvants for Neutrophil Immunometabolism.International journal of molecular sciences · 2026Review
- Tumor cell intrinsic mechanisms of immune escape.Cell communication and signaling : CCS · 2026Review
- Copper Transporter 1‑Mediated Deregulation of Copper Homeostasis Impacts MYC and Oxidative Phosphorylation Pathways and Increases the Sensitivity of Tumor Cells to Complex I Inhibitors.ACS pharmacology & translational science · 2026Article
- KRAS and MYC synergistic inhibition: a powerful strategy targeting KRAS-mutant cancers.Molecular cancer · 2026Review
- Cancer and aging: complex associations and therapeutic targets.Molecular biomedicine · 2026Review
- Liquiritin restores metabolic homeostasis in NAFLD by modulating AKT1/FOXO1 signaling.Frontiers in pharmacology · 2026Article
- Sequence Determinants of Allosteric Back-to-front Control of the Arf Nucleotide Switch.Journal of molecular biology · 2025Article
- Identification and validation of ARF6 for a potential prognostic biomarker of acute myeloid leukemia.Cancer cell international · 2025Article
- Acetylation-induced degradation of ECHS1 enhances BCAA accumulation and proliferation in KRAS-mutant colorectal cancer.Journal of experimental & clinical cancer research : CR · 2025Article
- Methuosis key gene ARF6 as a diagnostic, prognostic and immunotherapeutic marker for prostate cancer: based on a comprehensive pan-cancer multi-omics analysis.Discover oncology · 2025Article
- ARF6 Promotes AML Progression via Activation of PI3K/AKT/mTOR Signaling.Cancer medicine · 2025Article
- A sequencing-based screening method identifies regulators of EGFR signaling from nonviable mutants inScience signaling · 2025Article
- MYC and KRAS cooperation: from historical challenges to therapeutic opportunities in cancer.Signal transduction and targeted therapy · 2024Review
- Overcoming Resistance to Immune Checkpoint Blockade in Liver Cancer with Combination Therapy: Stronger Together?Seminars in liver disease · 2024Review
- Effect of acidosis on adipose-derived stem cell impairment and gene expression.Regenerative therapy · 2024Article
- A cell competition system with one gene expression from a single-copy gene in one cell.PloS one · 2024Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the KRAS gene and overexpression of protein products of the MYC and ARF6 genes occur frequently in cancer. Here, the inseparable relationships and cooperation of the protein products of these three genes in cancer malignancy and immune evasion are discussed. mRNAs encoded by these genes share the common feature of a G-quadruplex structure, which directs them to be robustly expressed when cellular energy production is increased. These three proteins are also functionally inseparable from each other, as follows. 1) KRAS induces MYC gene expression, and may also promote eIF4A-dependent MYC and ARF6 mRNA translation, 2) MYC induces the expression of genes involved in mitochondrial biogenesis and oxidative phosphorylation, and 3) ARF6 protects mitochondria from oxidative injury. ARF6 may moreover promote cancer invasion and metastasis, and also acidosis and immune checkpoint. Therefore, the inseparable relationships and cooperation of KRAS, MYC, and ARF6 appear to result in the activation of mitochondria and the driving of ARF6-based malignancy and immune evasion. Such adverse associations are frequent in pancreatic cancer, and appear to be further enhanced by TP53 mutations. Video Abstract.
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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.