ArticleThoracic cancer2022
Elevated BTG2 improves the radiosensitivity of non-small cell lung cancer (NSCLC) through apoptosis.
Article in Thoracic cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Effect of Reoxygenation on Radioresistance of Chronically Hypoxic A549 Non-Small Cell Lung Cancer (NSCLC) Cells Following X-Ray and Carbon Ion Exposure.International journal of molecular sciences · 2025Article
- A pan-cancer analysis of anti-proliferative protein family genes for therapeutic targets in cancer.Scientific reports · 2023Article
- Article
- Combination treatment of T1-44, a PRMT5 inhibitor with Vactosertib, an inhibitor of TGF-β signaling, inhibits invasion and prolongs survival in a mouse model of pancreatic tumors.Cell death & disease · 2023Article
- Downregulation of VRK1 Inhibits Progression of Lung Squamous Cell Carcinoma through DNA Damage.Canadian respiratory journal · 2023Article
- Elevated BTG2 improves the radiosensitivity of non-small cell lung cancer (NSCLC) through apoptosis.Thoracic cancer · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTo identify radio-responsive genes and explore the biological function of encoded proteins in non-small cell lung cancer (NSCLC).
methodsRadio-responsive genes in irradiated H460 cells were screened from microarray data deposited in the Gene Expression Omnibus (GEO) database. A quantitative real time polymerase chain reaction assay was used to detect the expression of candidate radio-responsive genes in irradiated cells. CCK-8 assay, EDU assay, clone formation assay, immunofluorescence and flow cytometry were conducted to evaluate the biological function of B cell translocation gene 2 (BTG2) in NSCLC.
resultsBioinformatic analysis using GES20549 showed that BTG2 was a radio-responsive gene in irradiated H460 cells. The mRNA expression level of BTG2 was lower in H460 cells compared with that in BEAS-2B normal lung epithelial cells. BTG2 expression was elevated upon IR exposure, in a dose-dependent but not a time-dependent manner. CCK-8 and EDU assays revealed that BTG2 overexpression inhibited the growth rate of irradiated cells. Clone formation showed that elevated BTG2 promoted DNA damage of irradiated H460 cells. The number of γ-H2AX foci induced by DNA damage was also markedly increased upon BTG2 overexpression. Flow cytometry showed that BTG2 increased IR-induced cell apoptosis.
conclusionsBTG2 may be a novel radio-responsive factor and a promising therapeutic target for radiotherapy of NSCLC.
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