ArticlePloS one2014
Elevated expression of AKR1C3 increases resistance of cancer cells to ionizing radiation via modulation of oxidative stress.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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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
33 citing papers in PubMed, 46 citations in OpenAlex.
- Phase 2 dose-expansion trial of OBI-3424, a DNA-alkylating prodrug, in patients with advanced solid tumors expressing AKR1C3.The oncologist · 2026Trial
- Cellular Senescence in Keloid Pathology: Mechanisms, Biomarkers, and Potential Therapeutic Targets.Biomedicines · 2026Review
- AKR1C3-PKM2-oxidative phosphorylation axis drives prostate cancer radioresistance via UBE2T upregulation.Cell death & disease · 2026Article
- Advances in ferroptosis for castration-resistant prostate cancer treatment: novel drug targets and combination therapy strategies.Prostate cancer and prostatic diseases · 2026Review
- Role of Aldo-Keto reductase family 1 member C in cancer progression: a special focus on the role of AKR1C1 in pancreatic cancer.Medical oncology (Northwood, London, England) · 2025Article
- Thermoresponsive antioxidant metal-free carbon nanodot hydrogel: An effective therapeutic approach for ocular surface disease.Science advances · 2025Article
- AKR1C3 enhances radioresistance in esophageal adenocarcinoma via inhibiting ferroptosis through suppressing TRIM21-mediated ubiquitination of HSPA5.Cell death & disease · 2025Article
- Human AKR1C3 binds agonists of GPR84 and participates in an expanded polyamine pathway.Cell chemical biology · 2025Article
- Coumarin-Based Aldo-Keto Reductase Family 1C (AKR1C) 2 and 3 Inhibitors.ChemMedChem · 2024Article
- Aldo-keto reductase family 1 member C3 mediates radioresistance of esophageal cancer cells through suppressing MAPK and AKT signaling.BMC cancer · 2024Article
- AKR1C3 promotes progression and mediates therapeutic resistance by inducing epithelial-mesenchymal transition and angiogenesis in small cell lung cancer.Translational oncology · 2024Article
- AKR1C3 in carcinomas: from multifaceted roles to therapeutic strategies.Frontiers in pharmacology · 2024Review
- Upregulation of AKR1C3 in Sodium Butyrate Treated G361 Cell.Annals of dermatology · 2023Article
- Possible New Histological Prognostic Index for Large B-Cell Lymphoma.Journal of clinical medicine · 2023Article
- Phase 1 dose-escalation study evaluating the safety, pharmacokinetics, and clinical activity of OBI-3424 in patients with advanced or metastatic solid tumors.British journal of cancer · 2023Article
- COVID-19: Focusing on the Link between Inflammation, Vitamin D, MAPK Pathway and Oxidative Stress Genetics.Antioxidants (Basel, Switzerland) · 2023Article
- A prognosis model for predicting immunotherapy response of esophageal cancer based on oxidative stress-related signatures.Oncology research · 2023Article
- Induction and assessment of persistent radioresistance in murine leukocytesBiochemistry and biophysics reports · 2022Article
- Article
- Expression of AKR1C3, β-Catenin and LEF1 in Esophageal Squamous Cell Carcinoma and the Relationship with Radiation Resistance.Iranian journal of public health · 2021Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
With the aim to elucidate the etiology of radioresistance, we explored the genetic alterations in non-radioresistant vs. resistant esophageal cancer cells acquired by long-term fractionated radiation. We found AKR1C3, an aldo-keto reductase expressed seldom in most human tissues, expressed higher in radioresistance-acquired cells. Suppression of AKR1C3 via RNAi or its chemical inhibitors restored the sensitivity of the acquired tumor cells and xenograft BALB/c nude mice to ionizing radiation (IR). Cellular monitoring of the oxidative stress in the AKR1C3-elevated cells indicated that IR-induced ROS accumulation and the concomitant DNA damage was significantly alleviated, and such protective consequence disappeared upon AKR1C3 knockdown. These findings uncover the potential involvement of AKR1C3 in removal of cellular ROS and explain, at least partially, the acquired radioresistance by AKR1C3 overexpression. A retrospective analysis of esophageal carcinomas also indicated a significant expression of AKR1C3 in radio-resistant but not radio-sensitive surgical samples. Our study may provide a potential biomarker for predicting prognosis of radiotherapy and even direct a targeted therapy for esophageal cancer and other tumors.
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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.