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Elevated BTG2 improves the radiosensitivity of non‐small cell lung cancer (NSCLC) through apoptosis

BACKGROUND: To identify radio‐responsive genes and explore the biological function of encoded proteins in non‐small cell lung cancer (NSCLC). METHODS: Radio‐responsive genes in irradiated H460 cells were screened from microarray data deposited in the Gene Expression Omnibus (GEO) database. A quantit...

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Autores principales: Zhu, Changchun, Zhang, Songling, Xue, Aiying, Feng, Guoxing, Fan, Saijun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley & Sons Australia, Ltd 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9108063/
https://www.ncbi.nlm.nih.gov/pubmed/35388633
http://dx.doi.org/10.1111/1759-7714.14410
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author Zhu, Changchun
Zhang, Songling
Xue, Aiying
Feng, Guoxing
Fan, Saijun
author_facet Zhu, Changchun
Zhang, Songling
Xue, Aiying
Feng, Guoxing
Fan, Saijun
author_sort Zhu, Changchun
collection PubMed
description BACKGROUND: To identify radio‐responsive genes and explore the biological function of encoded proteins in non‐small cell lung cancer (NSCLC). METHODS: Radio‐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. RESULTS: Bioinformatic 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. CONCLUSIONS: BTG2 may be a novel radio‐responsive factor and a promising therapeutic target for radiotherapy of NSCLC.
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spelling pubmed-91080632022-05-20 Elevated BTG2 improves the radiosensitivity of non‐small cell lung cancer (NSCLC) through apoptosis Zhu, Changchun Zhang, Songling Xue, Aiying Feng, Guoxing Fan, Saijun Thorac Cancer Original Articles BACKGROUND: To identify radio‐responsive genes and explore the biological function of encoded proteins in non‐small cell lung cancer (NSCLC). METHODS: Radio‐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. RESULTS: Bioinformatic 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. CONCLUSIONS: BTG2 may be a novel radio‐responsive factor and a promising therapeutic target for radiotherapy of NSCLC. John Wiley & Sons Australia, Ltd 2022-04-07 2022-05 /pmc/articles/PMC9108063/ /pubmed/35388633 http://dx.doi.org/10.1111/1759-7714.14410 Text en © 2022 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Original Articles
Zhu, Changchun
Zhang, Songling
Xue, Aiying
Feng, Guoxing
Fan, Saijun
Elevated BTG2 improves the radiosensitivity of non‐small cell lung cancer (NSCLC) through apoptosis
title Elevated BTG2 improves the radiosensitivity of non‐small cell lung cancer (NSCLC) through apoptosis
title_full Elevated BTG2 improves the radiosensitivity of non‐small cell lung cancer (NSCLC) through apoptosis
title_fullStr Elevated BTG2 improves the radiosensitivity of non‐small cell lung cancer (NSCLC) through apoptosis
title_full_unstemmed Elevated BTG2 improves the radiosensitivity of non‐small cell lung cancer (NSCLC) through apoptosis
title_short Elevated BTG2 improves the radiosensitivity of non‐small cell lung cancer (NSCLC) through apoptosis
title_sort elevated btg2 improves the radiosensitivity of non‐small cell lung cancer (nsclc) through apoptosis
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9108063/
https://www.ncbi.nlm.nih.gov/pubmed/35388633
http://dx.doi.org/10.1111/1759-7714.14410
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