ArticleNucleic acids research2021
Oncogenic KRAS drives radioresistance through upregulation of NRF2-53BP1-mediated non-homologous end-joining repair.
Article in Nucleic acids research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 67 citations in OpenAlex.
- Liquid biopsy: current applications and future directions.Molecular biomedicine · 2026Review
- Challenges and opportunities in combining radiotherapy and immunotherapy for localized pancreatic cancer.Nature reviews. Gastroenterology & hepatology · 2026Review
- RAS signaling at the crossroads of radioresistance and tumor immunity.Journal for immunotherapy of cancer · 2026Review
- Targeting programmed cell death: a novel therapeutic paradigm for cancer based on mode-of-death classification.Apoptosis : an international journal on programmed cell death · 2026Review
- Radiosensitization of Glioblastoma by the K-ras Inhibitor RMC-6236.bioRxiv : the preprint server for biology · 2026Article
- Article
- Local Control With Reduced-Dose Radiation Therapy for High-Risk Neuroblastoma: Results From a Prospective Clinical Trial.International journal of radiation oncology, biology, physics · 2026Article
- KRAS Mutation Status as a Prognostic Marker and Predictor of Therapy Response in Colorectal Cancer: an NCDB Analysis.Journal of gastrointestinal cancer · 2026Article
- Loss of MicroRNA-29b promotes DNMT3b-mediated STING downregulation to attenuate radiotherapy-induced antitumor immunity in KRAS-mutated colorectal cancer.NPJ precision oncology · 2026Article
- Radiogenomics and the DNA damage response: opportunities for biomarker-guided radiosensitization in pancreatic cancer.Frontiers in oncology · 2026Review
- Geno-guided targeting of ferroptosis: a multi-layered network to overcome radioresistance in lung cancer.Frontiers in cell and developmental biology · 2026Review
- Impact of RAS-MAPK Pathway Genetic Alterations on Radiotherapy Response in Metastatic Lung Adenocarcinoma.JCO precision oncology · 2025Article
- The Unfolded Protein Response-Novel Mechanisms, Challenges, and Key Considerations for Therapeutic Intervention.Cancers · 2025Review
- Article
- The Impact of RAS/BRAF Mutation on Pathological Complete Response After Total Neoadjuvant Therapy in Rectal Cancer.Annals of surgical oncology · 2025Article
- KRAS-induced STN1 (OBFC1) promotes proper CTC1-STN1-TEN1 complex-independent DNA double-strand break repair and cell cycle checkpoint maintenance in pancreatic cancer.Nucleic acids research · 2025Article
- Proteomic Analysis of FFPE Tissue Samples Identifies Potential Molecular Mechanisms Mediating Resistance to Radiotherapy in Rectal Cancer.Journal of proteome research · 2025Article
- Review
- Discovery and Characterization of Small Molecule Inhibitors Targeting Exonuclease 1 for Homologous Recombination-Deficient Cancer Therapy.ACS chemical biology · 2025Article
- Oncogenic stress response mechanisms as new therapeutic targets in cancer treatment: A review.Medicine · 2025Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
KRAS-activating mutations are oncogenic drivers and are correlated with radioresistance of multiple cancers, including colorectal cancer, but the underlying precise molecular mechanisms remain elusive. Herein we model the radiosensitivity of isogenic HCT116 and SW48 colorectal cancer cell lines bearing wild-type or various mutant KRAS isoforms. We demonstrate that KRAS mutations indeed lead to radioresistance accompanied by reduced radiotherapy-induced mitotic catastrophe and an accelerated release from G2/M arrest. Moreover, KRAS mutations result in increased DNA damage response and upregulation of 53BP1 with associated increased non-homologous end-joining (NHEJ) repair. Remarkably, KRAS mutations lead to activation of NRF2 antioxidant signaling to increase 53BP1 gene transcription. Furthermore, genetic silencing or pharmacological inhibition of KRAS, NRF2 or 53BP1 attenuates KRAS mutation-induced radioresistance, especially in G1 phase cells. These findings reveal an important role for a KRAS-induced NRF2-53BP1 axis in the DNA repair and survival of KRAS-mutant tumor cells after radiotherapy, and indicate that targeting NRF2, 53BP1 or NHEJ may represent novel strategies to selectively abrogate KRAS mutation-mediated radioresistance.
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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.