Cargando…
自噬对人肺腺癌A549细胞放疗敏感性的影响
BACKGROUND AND OBJECTIVE: Radiotherapy is an important treatment for lung cancer. The poor prognosis of lung cancer is largely caused by the high recurrence rate and metastasis of the tumor. Autophagy, which can be induced by radiotherapy, might be associated with DNA repair. The aim of this study i...
Formato: | Online Artículo Texto |
---|---|
Lenguaje: | English |
Publicado: |
中国肺癌杂志编辑部
2016
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5973450/ https://www.ncbi.nlm.nih.gov/pubmed/27978864 http://dx.doi.org/10.3779/j.issn.1009-3419.2016.12.01 |
_version_ | 1783326636246040576 |
---|---|
collection | PubMed |
description | BACKGROUND AND OBJECTIVE: Radiotherapy is an important treatment for lung cancer. The poor prognosis of lung cancer is largely caused by the high recurrence rate and metastasis of the tumor. Autophagy, which can be induced by radiotherapy, might be associated with DNA repair. The aim of this study is to investigate whether activating autophagy using rapamycin can enhance the radiosensitivity of lung cancer cells and clarify the association of autophagy with DNA repair. METHODS: The human adenocarcinoma A549 cell line was selected as the experimental subject. The specimens were divided into three groups: control (N), radiation (R), and Rapamycin and radiation (R+RAPA). The protein levels of γ-H2AX, Rad51, Ku70/Ku80, p62, and LC3 were determined by Western blot. Autophagosome was observed under a transmission electron microscope, and SF was determined by colony formation assay. RESULTS: Compared with group R, the activity of autophagy and the protein expression levels of Rad51 and Ku70/80 were remarkably increased in group R+RAPA. CONCLUSIONS: The radiosensitivity of lung cancer can be promoted by activating autophagy via treatment with Rapamycin, and the process may be associated with DNA repair. |
format | Online Article Text |
id | pubmed-5973450 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | 中国肺癌杂志编辑部 |
record_format | MEDLINE/PubMed |
spelling | pubmed-59734502018-07-06 自噬对人肺腺癌A549细胞放疗敏感性的影响 Zhongguo Fei Ai Za Zhi 基础研究 BACKGROUND AND OBJECTIVE: Radiotherapy is an important treatment for lung cancer. The poor prognosis of lung cancer is largely caused by the high recurrence rate and metastasis of the tumor. Autophagy, which can be induced by radiotherapy, might be associated with DNA repair. The aim of this study is to investigate whether activating autophagy using rapamycin can enhance the radiosensitivity of lung cancer cells and clarify the association of autophagy with DNA repair. METHODS: The human adenocarcinoma A549 cell line was selected as the experimental subject. The specimens were divided into three groups: control (N), radiation (R), and Rapamycin and radiation (R+RAPA). The protein levels of γ-H2AX, Rad51, Ku70/Ku80, p62, and LC3 were determined by Western blot. Autophagosome was observed under a transmission electron microscope, and SF was determined by colony formation assay. RESULTS: Compared with group R, the activity of autophagy and the protein expression levels of Rad51 and Ku70/80 were remarkably increased in group R+RAPA. CONCLUSIONS: The radiosensitivity of lung cancer can be promoted by activating autophagy via treatment with Rapamycin, and the process may be associated with DNA repair. 中国肺癌杂志编辑部 2016-12-20 /pmc/articles/PMC5973450/ /pubmed/27978864 http://dx.doi.org/10.3779/j.issn.1009-3419.2016.12.01 Text en 版权所有©《中国肺癌杂志》编辑部2016 https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY 3.0) License. See: https://creativecommons.org/licenses/by/3.0/ |
spellingShingle | 基础研究 自噬对人肺腺癌A549细胞放疗敏感性的影响 |
title | 自噬对人肺腺癌A549细胞放疗敏感性的影响 |
title_full | 自噬对人肺腺癌A549细胞放疗敏感性的影响 |
title_fullStr | 自噬对人肺腺癌A549细胞放疗敏感性的影响 |
title_full_unstemmed | 自噬对人肺腺癌A549细胞放疗敏感性的影响 |
title_short | 自噬对人肺腺癌A549细胞放疗敏感性的影响 |
title_sort | 自噬对人肺腺癌a549细胞放疗敏感性的影响 |
topic | 基础研究 |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5973450/ https://www.ncbi.nlm.nih.gov/pubmed/27978864 http://dx.doi.org/10.3779/j.issn.1009-3419.2016.12.01 |
work_keys_str_mv | AT zìshìduìrénfèixiànáia549xìbāofàngliáomǐngǎnxìngdeyǐngxiǎng AT zìshìduìrénfèixiànáia549xìbāofàngliáomǐngǎnxìngdeyǐngxiǎng AT zìshìduìrénfèixiànáia549xìbāofàngliáomǐngǎnxìngdeyǐngxiǎng AT zìshìduìrénfèixiànáia549xìbāofàngliáomǐngǎnxìngdeyǐngxiǎng AT zìshìduìrénfèixiànáia549xìbāofàngliáomǐngǎnxìngdeyǐngxiǎng AT zìshìduìrénfèixiànáia549xìbāofàngliáomǐngǎnxìngdeyǐngxiǎng |