NDLI: 125I seeds irradiation inhibits tumor growth and induces apoptosis by Ki-67, P21, survivin, livin and caspase-9 expression in lung carcinoma xenografts

Content Provider	Springer Nature : BioMed Central
Author	Jin, Qing Lin, Cunzhi Zhu, Xinhong Cao, Yiwei Guo, Caihong Wang, Lijun
Abstract	Background Lung cancer is a fatal disease and a serious health problem worldwide. Patients are usually diagnosed at an advanced stage, and the effectiveness of chemotherapy for such patients is very limited. Iodine 125 seed (125I) irradiation can be used as an important adjuvant treatment for lung carcinoma. The purpose of this study was to examine the role of irradiation by 125I seeds in human lung cancer xenograft model and to determine the underlying mechanisms involved, with a focus on apoptosis. Methods 40 mice with A549 lung adenocarcinoma xenografts were randomly divided into 4 groups: control group (n = 10), sham seed (0 mCi) implant group (n = 10), 125I seed (0.6 mCi) implant group (n = 10) and 125I seed (0.8 mCi) implant group (n = 10), respectively. The body weight and tumor volume, were recorded every 4 days until the end of the study. Apoptotic cells were checked by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay and activities of caspase-3 and caspase-8 enzyme were tested. Expression of P21, survivin, livin, caspase-9 and proliferating cell nuclear antigen (Ki-67) was detected with immunohistochemical staining. Results The results of TUNEL staining assays showed that 125I seed irradiation suppresses the growth of lung cancer xenografts in nude mice and induced apoptosis. The activity of caspase-3 and caspase-8 was significantly higher. The expression levels Ki67, survivin and livin were substantially downregulated, while P21 and caspase-9 protein expression were significantly increased following 125I seed irradiation. This study revealed that 125I seed irradiation could significantly change apoptosis-related protein in human lung cancer xenografts. Conclusions Overall, our study demonstrates that radiation exposure by 125I seeds could be a new treatment option for lung cancer.
Related Links	https://ro-journal.biomedcentral.com/counter/pdf/10.1186/s13014-020-01682-5.pdf
Ending Page	10
Page Count	10
Starting Page	1
File Format	HTM / HTML
DOI	10.1186/s13014-020-01682-5
Journal	Radiation Oncology
Issue Number	1
Volume Number	15
Language	English
Publisher	BioMed Central
Publisher Date	2020-10-15
Access Restriction	Open
Subject Keyword	Cancer Research Oncology Radiotherapy Imaging Radiology 125I seeds Lung carcinoma Apoptosis Ki-67 P21
Content Type	Text
Resource Type	Article
Subject	Radiology, Nuclear Medicine and Imaging Oncology
Journal Impact Factor	3.3/2023
5-Year Journal Impact Factor	3.6/2023

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Correction to: 125I seeds irradiation inhibits tumor growth and induces apoptosis by Ki-67, P21, survivin, livin and caspase-9 expression in lung carcinoma xenografts

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X-radiation inhibits histone deacetylase 1 and 2, upregulates Axin expression and induces apoptosis in non-small cell lung cancer

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125I seed irradiation induces up-regulation of the genes associated with apoptosis and cell cycle arrest and inhibits growth of gastric cancer xenografts

125I seeds irradiation inhibits tumor growth and induces apoptosis by Ki-67, P21, survivin, livin and caspase-9 expression in lung carcinoma xenografts

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Correction to: 125I seeds irradiation inhibits tumor growth and induces apoptosis by Ki-67, P21, survivin, livin and caspase-9 expression in lung carcinoma xenografts

125I seed irradiation induces apoptosis and inhibits angiogenesis by decreasing HIF-1α and VEGF expression in lung carcinoma xenografts.

125I seed irradiation induces up-regulation of the genes associated with apoptosis and cell cycle arrest and inhibits growth of gastric cancer xenografts

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125I seeds irradiation inhibits tumor growth and induces apoptosis by Ki-67, P21, survivin, livin and caspase-9 expression in lung carcinoma xenografts