ArticleRadiation oncology (London, England)2013
Combined effects of C225 and 125-iodine seed radiation on colorectal cancer cells.
Article in Radiation oncology (London, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Survival of patients with advanced pancreatic cancer after iodine125 seeds implantation brachytherapy: A meta-analysis.Medicine · 2017Pooled it
- Iodine-125 seed represses the growth and facilitates the apoptosis of colorectal cancer cells by suppressing the methylation of miR-615 promoter.BMC cancer · 2022Article
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- Evaluation of Iodine-125 Interstitial Brachytherapy Using Micro-Positron Emission Tomography/Computed Tomography with 18F-Fluorodeoxyglucose in Hepatocellular Carcinoma HepG2 Xenografts.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Iodine-125 interstitial brachytherapy reduces tumor growth via Warburg effect inhibition in non-small cell lung cancer A549 ×enografts.Oncology letters · 2018Article
- c-Src/Cav1-dependent activation of the EGFR by Dsg2.Oncotarget · 2016Article
- The Protective Roles of ROS-Mediated Mitophagy onOxidative medicine and cellular longevity · 2016Article
- Article
- InterstitialTechnology in cancer research & treatmentArticle
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6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTo characterize the effect of combined treatment of the anti-epidermal growth factor receptor (EGFR) monoclonal antibody C225 and 125-iodine (125I) seed radiation in human colorectal cancer.
methodsWe treated LS180 cells with 125I continuous low dose rate radiation in the presence and absence of 100 nM C225. The clonogenic capacity, cellular proliferation, cell cycle distribution, apoptosis, and molecular pathways of the cells following the treatments were analyzed in vitro.
resultsThe sensitizer enhancement ratio of C225 was approximately 1.4. Treatment with C225 and radiation alone produced significant inhibition of cell growth, but combination therapy produced greater inhibition than either treatment administered alone. C225 increased the radiation-induced apoptosis and the fraction of γ-H2AX foci positive cells at 48 h after treatment. The Akt phosphorylation level was lower in the cells receiving the combination treatment than in the cells treated with radiation or C225 alone.
conclusionsThese findings indicate that C225 sensitizes LS180 cells to 125I seed radiation. Growth inhibition is mediated by inducing apoptosis and not cell cycle arrest. Additionally, we confirmed that C225 impairs DNA repair by reducing the cellular level of the DNA-PKcs and Ku70 proteins. Furthermore, the inhibition of Akt signaling activation may be responsible for the C225-mediated radiosensitization.
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