ArticleWorld journal of oncology2018
Inhibition of ERK1/2 or AKT Activity Equally Enhances Radiation Sensitization in B16F10 Cells.
Article in World journal of oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Quinoline conjugates for enhanced antimalarial activity: a review on synthesis by molecular hybridization and structure-activity relationship (SAR) investigation.American journal of translational research · 2025Review
- Acute and chronic toxicity studies on ethanolic leaf extracts ofInternational journal of biochemistry and molecular biology · 2022Article
- Hypoglycemic and hypolipidemic effects of Garcinia cambogia extracts in streptozotocin-nicotinamide induced diabetic rat model.International journal of clinical and experimental pathology · 2022Article
- Cilostazol eliminates radiation-resistant glioblastoma by re-evoking big conductance calcium-activated potassium channel activity.American journal of cancer research · 2021Article
- Serum Ischemia-Modified Albumin, Fibrinogen, High Sensitivity C- Reactive Proteins in Type-2 Diabetes Mellitus without Hypertension and Diabetes Mellitus with Hypertension: A Case-Control Study.Reports of biochemistry & molecular biology · 2020Article
- Oxidative stress in cervical cancer and its response to chemoradiation.Turkish journal of obstetrics and gynecology · 2019Article
- HDAC2 Inhibitor Valproic Acid Increases Radiation Sensitivity of Drug-Resistant Melanoma Cells.Medical sciences (Basel, Switzerland) · 2019Article
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe aim of the study was to evaluate the radiation sensitizing ability of ERK1/2, PI3K-AKT and JNK inhibitors in highly radiation resistant and metastatic B16F10 cells which carry wild-type
methodsMouse melanoma cell line B16F10 was exposed to 1.0, 2.0 and 3.0 Gy of electron beam radiation. Phosphorylated ERK1/2, AKT and JNK levels were estimated by ELISA. Cells were exposed to 2.0 and 3.0 Gy of radiation with or without prior pharmacological inhibition of ERK1/2, AKT as well as JNK pathways. Cell death induced by radiation as well as upon inhibition of these pathways was measured by TUNEL assay using flow cytometry.
resultsExposure of B16F10 cells to 1.0, 2.0 and 3.0 Gy of electron beam irradiation triggered an increase in all the three phosphorylated proteins compared to sham-treated and control groups. B16F10 cells pre-treated with either ERK1/2 or AKT inhibitors equally enhanced radiation-induced cell death at 2.0 as well as 3.0 Gy (P < 0.001), while inhibition of JNK pathway increased radiation-induced cell death to a lesser extent. Interestingly combined inhibition of ERK1/2 or AKT pathways did not show additional cell death compared to individual ERK1/2 or AKT inhibition. This indicates that ERK1/2 or AKT mediates radiation resistance through common downstream molecules in B16F10 cells.
conclusionsEven without activating mutations in
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