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Radiation-Induced Bystander Effect on the Genome of Bone Marrow Mesenchymal Stem Cells in Lung Cancer  ( SCI-EXPANDED收录)   被引量:5

文献类型:期刊文献

英文题名:Radiation-Induced Bystander Effect on the Genome of Bone Marrow Mesenchymal Stem Cells in Lung Cancer

作者:Zhang, Yi-Ming[1];Zhang, Li-Ying[1,2];Li, Yang-Yang[1];Zhou, Heng[3,4];Miao, Zhi-Ming[1];Liu, Zhi-Wei[1];Zhou, Gu-Cheng[1];Zhou, Ting[1];Niu, Fan[1];Li, Jing[1];Hong, Tao[1];He, Jin-Peng[3,4];Ding, Nan[3,4];Zhang, Ya-Nan[3,4];Hua, Jun-Rui[3,4];Wang, Ju-Fang[3,4];Liu, Yong-Qi[1,5]

第一作者:张艺梦

通信作者:Liu, YQ[1];Wang, JF[2];Liu, YQ[3]

机构:[1]Gansu Univ Chinese Med, Prov Level Key Lab Mol Med Major Dis & Prevent & T, Lanzhou, Peoples R China;[2]Gansu Inst Cardiovasc Dis, Lanzhou, Peoples R China;[3]Chinese Acad Sci, Key Lab Space Radiobiol Gansu Prov, Lanzhou, Peoples R China;[4]Chinese Acad Sci, Key Lab Heavy Ion Radiat Biol & Med, Inst Modern Phys, Lanzhou, Peoples R China;[5]Minist Educ, Key Lab Dunhuang Med, Lanzhou, Peoples R China

第一机构:甘肃中医药大学

通信机构:[1]corresponding author), Gansu Univ Chinese Med, Prov Level Key Lab Mol Med Major Dis & Prevent & T, Lanzhou, Peoples R China;[2]corresponding author), Chinese Acad Sci, Key Lab Space Radiobiol Gansu Prov, Lanzhou, Peoples R China;[3]corresponding author), Minist Educ, Key Lab Dunhuang Med, Lanzhou, Peoples R China.|[10735]甘肃中医药大学;

年份:2023

卷号:38

期号:10-12

起止页码:747

外文期刊名:ANTIOXIDANTS & REDOX SIGNALING

收录:;Scopus(收录号:2-s2.0-85149418826);WOS:【SCI-EXPANDED(收录号:WOS:000894741100001)】;

基金:This study was funded by the National Natural Science Foundation of China (Nos. 81973595, 82004094, and 82260882) and the Basic Research Innovation Group (No. 20JR10RA332).

语种:英文

外文关键词:RIBE; lung cancer; BMSCs; genome instability; TNF-alpha; TGF-beta 1; HIF-1 alpha

摘要:Aims: Radiation by-radiation effect (RIBE) can induce the genomic instability of bone marrow mesenchymal stem cells (BMSCs) adjacent to lung cancer, and this effect not only exists in the short-term, but also accompanies it in the long-term, but its specific mechanism is not clear. Our goal is to explore the similarities and differences in the mechanism of genomic damage in tumor-associated BMSCs induced by short-term and long-term RIBE, and to provide a theoretical basis for adjuvant drugs for protection against RIBE at different clinical time periods. [GRAPHICS] Results: We found that both short- and long-term RIBE induced genomic instability. We could show a high expression of TGF-beta 1, TNF-alpha, and HIF-1 alpha in tumor-associated BMSCs after short-term RIBE whereas only TNF-alpha and HIF-1 alpha expression was increased in long-term RIBE. We further confirmed that genomic instability is associated with the activation of the HIF-1 alpha pathway and that this is mediated by TNF-alpha and TGF-beta 1. In addition, we found differences in the mechanisms of genomic instability in the considered RIBE windows of analysis. In short-term RIBE, both TNF-alpha and TGF-beta 1 play a role, whereas only TNF-alpha plays a decisive role in long-term RIBE. In addition, there were differences in BMSC recruitment and genomic instability of different tissues with a more pronounced expression in tumor and bone marrow than compared to lung. Innovation and Conclusion: We could show dynamic changes in the expression of the cytokines TGF-beta 1 and TNF-alpha during short- and long-term RIBE. The differential expression of the two is the key to causing the genomic damage of tumor-associated BMSCs in the considered windows of analysis. Therefore, these results may serve as a guideline for the administration of radiation protection adjuvant drugs at different clinical stages.

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