ArticleCell death & disease2025
ROBO1 enhanced esophageal carcinoma cell radioresistance through accelerating G3BP2-mediated eIF3A degradation.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Review
- Repression of ROBO1 Enhances Cisplatin Sensitivity in Hypermethylated Subtype of HPV-Positive Head and Neck Carcinoma.Cancer science · 2026Article
- Research Progress on the Biological Function, Disease-Driving Mechanism and Clinical Targeting Strategies of G3BP2.Molecules (Basel, Switzerland) · 2026Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Radiotherapy, as a vital means of esophageal cancer treatment, has benefited countless cancer patients, but owing to the occurrence of radio-resistance, its therapeutic efficiency has been dramatically mitigated. Discovering key biomarkers governing radio-tolerance in esophageal cancer and revealing their inherent molecular mechanisms will be of great significance for clinical cancer treatment. Here, we have found roundabout guidance receptor 1 (ROBO1) was significantly upregulated in esophageal cancerous tissues and showed enhanced expression with the development of cancer staging. Cellular experiments demonstrated ROBO1 directly interacted with eukaryotic translation initiation factor 3A (eIF3A) and accelerated its degradation in esophageal cancer cells after irradiation treatment. Mass spectrum analysis further revealed that in response to irradiation, ROBO1, eIF3A and G3BP2 (Ras GTPase-activating protein-binding protein 2) formed a hetero-complex and triggered lysosomes-mediated protein degradation. Knocking down of G3BP2 abrogated the influence of ROBO1 on eIF3A instability. Besides, ROBO1-mediated eIF3A degradation interrupted P53 translation process which in turn provoked downstream mTOR signaling and increased DNA repair associated genes expressions, resulting in radio-resistance enhancement in cancer cells. In conclusion, our findings revealed a novel role of eIF3A in modulating P53/mTOR signaling activity and provided a drug candidate (ROBO1) for overcoming radio-resistance in esophageal cancer.
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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 Socratic graph.