ArticlePloS one2014
Beclin 1 and UVRAG confer protection from radiation-induced DNA damage and maintain centrosome stability in colorectal cancer cells.
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 52 papers, 1 of them a synthesis that pooled it.
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
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- Pooled it
- Nuclear PI3P produced by the Beclin-1/Vps34 complex regulates DNA mismatch repair.Nucleic acids research · 2026Article
- Beyond self‑eating: Emerging autophagy‑independent functions for the autophagy molecules in cancer (Review).International journal of oncology · 2024Review
- NLRX1 Inhibits LPS-Induced Microglial Death via Inducing p62-Dependent HO-1 Expression, Inhibiting MLKL and Activating PARP-1.Antioxidants (Basel, Switzerland) · 2024Article
- Structured testing of genetic association with mixed clinical outcomes.Genetic epidemiology · 2024Article
- The nonautophagic functions of autophagy-related proteins.Autophagy · 2024Review
- Role of protein degradation systems in colorectal cancer.Cell death discovery · 2024Review
- Beclin-1: a therapeutic target at the intersection of autophagy, immunotherapy, and cancer treatment.Frontiers in immunology · 2024Review
- Targeting autophagy and beyond: Deconvoluting the complexity of Beclin-1 from biological function to cancer therapy.Acta pharmaceutica Sinica. B · 2023Review
- Autophagy: A challengeable paradox in cancer treatment.Cancer medicine · 2023Review
- PLP2 Could Be a Prognostic Biomarker and Potential Treatment Target in Glioblastoma Multiforme.Pharmacogenomics and personalized medicine · 2023Article
- Inhibition of Autophagy Promotes the Elimination of Liver Cancer Stem Cells by CD133 Aptamer-Targeted Delivery of Doxorubicin.Biomolecules · 2022Article
- Nrf2 Pathway and Autophagy Crosstalk: New Insights into Therapeutic Strategies for Ischemic Cerebral Vascular Diseases.Antioxidants (Basel, Switzerland) · 2022Review
- Effect of Autophagy Inhibitors on Radiosensitivity in DNA Repair-Proficient and -Deficient Glioma Cells.Medicina (Kaunas, Lithuania) · 2022Article
- A novel ATG5 interaction with Ku70 potentiates DNA repair upon genotoxic stress.Scientific reports · 2022Article
- Radiotherapy as a tool to elicit clinically actionable signalling pathways in cancer.Nature reviews. Clinical oncology · 2022Review
- Autophagy-related Proteins in Genome Stability: Autophagy-Dependent and Independent Actions.International journal of biological sciences · 2022Review
- Establishment and validation of five autophagy-related signatures for predicting survival and immune microenvironment in glioma.Genes & genomics · 2022Article
- Targeting Cytoprotective Autophagy to Enhance Anticancer Therapies.Frontiers in oncology · 2021Review
- The Impact of Aging on Macroautophagy in the Pre-ovulatory Mouse Oocyte.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Beclin 1 interacts with UV-irradiation-resistance-associated gene (UVRAG) to form core complexes that induce autophagy. While cells with defective autophagy are prone to genomic instability that contributes to tumorigenesis, it is unknown whether Beclin1 or UVRAG can regulate the DNA damage/repair response to cancer treatment in established tumor cells. We found that siRNA knockdown of Beclin 1 or UVRAG can increase radiation-induced DNA double strand breaks (DSBs), shown by pATM and γH2Ax, and promote colorectal cancer cell death. Furthermore, knockdown of Beclin 1, UVRAG or ATG5 increased the percentage of irradiated cells with nuclear foci expressing 53BP1, a marker of nonhomologous end joining but not RAD51 (homologous recombination), compared to control siRNA. Beclin 1 siRNA was shown to attenuate UVRAG expression. Cells with a UVRAG deletion mutant defective in Beclin 1 binding showed increased radiation-induced DSBs and cell death compared to cells with ectopic wild-type UVRAG. Knockdown of Beclin 1 or UVRAG, but not ATG5, resulted in a significant increase in centrosome number (γ-tubulin staining) in irradiated cells compared to control siRNA. Taken together, these data indicate that Beclin 1 and UVRAG confer protection against radiation-induced DNA DSBs and may maintain centrosome stability in established tumor cells.
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What OpenQuestion holds
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.