Leukemogenic aml1-eto fusion protein increases carcinogen-dna adduct formation with upregulated expression of cytochrome p450-1a1 gene
文献类型:期刊论文
作者 | Xu, Min; Li, Dao; Lu, Ying; Chen, Guo-Qiang |
刊名 | Experimental hematology
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出版日期 | 2007-08-01 |
卷号 | 35期号:8页码:1249-1255 |
ISSN号 | 0301-472X |
DOI | 10.1016/j.exphem.2007.04.018 |
通讯作者 | Chen, guo-qiang(chengq@shsmu.edu.cn) |
英文摘要 | Objective. aml1-eto fusion protein is a product of chromosome translocation t(8;21) frequently occurred in acute myeloid leukemia (aml), but its sole expression appears to fail to cause overt leukemia in vivo. in this study, we investigated whether aml1-eto expression impinged on action of chemical carcinogens-dna adduct formation. materials and methods. aml1-eto fusion protein was conditionally induced in engineered u937-a/e 9/14/18 cells. the formation of polycyclic aromatic hydrocarbon (pah)-dna adducts and the expression of pah-metabolizing enzymes cytochrome p450 (cyp) 1a1 and arythydrocarbon receptor (ahr) were detected by western blot and/or quantitative rt-pcr. luciferase reporter system was used to detect the regulation of aml1-eto on cyp1a1 transcription. results. our results showed that aml1-eto induction significantly increased the formation of carcinogen benzopyrene-dna adducts in leukemic cells. in line with the effect, we also found that aml1-eto induction upregulated cyp1a1 expression, which was dependent on aml1-binding motif in the promotor of cyp1a1 gene. additionally, aml1-eto protein also increased ahr expression, a ligand-activated transcription factor that mediates pahsinduced cyp1a1 gene expression. conclusion. these data, combined with its inhibitory effect on dna repair as reported previously, propose that the presence of aml1-eto increases the susceptibility of cells to chemical carcinogens, which favors the development of additional genetic alterations. (c) 2007 iseh - society for hematology and stem cells. published by elsevier inc. |
WOS关键词 | ACUTE MYELOID-LEUKEMIA ; ACUTE LYMPHOBLASTIC-LEUKEMIA ; SMALL INTERFERING RNAS ; CELL-DIFFERENTIATION ; T(8/21) LEUKEMIA ; CYP1A1 ; TRANSCRIPTION ; INDUCTION ; CANCER ; SUSCEPTIBILITY |
WOS研究方向 | Hematology ; Research & Experimental Medicine |
WOS类目 | Hematology ; Medicine, Research & Experimental |
语种 | 英语 |
WOS记录号 | WOS:000248641000010 |
出版者 | ELSEVIER SCIENCE INC |
URI标识 | http://www.irgrid.ac.cn/handle/1471x/2383256 |
专题 | 中国科学院大学 |
通讯作者 | Chen, Guo-Qiang |
作者单位 | 1.Shanghai Jiao Tong Univ, Sch Med, Dept Pathophysiol, Key Lab Cell Differentiat & Apoptosis,Minist Educ, Shanghai 200025, Peoples R China 2.Shanghai Jiao Tong Univ, Sch Med, Inst Hlth Sci, Shanghai Inst Biol Sci, Shanghai 200025, Peoples R China 3.Chinese Acad Sci, Grad Sch, Shanghai, Peoples R China |
推荐引用方式 GB/T 7714 | Xu, Min,Li, Dao,Lu, Ying,et al. Leukemogenic aml1-eto fusion protein increases carcinogen-dna adduct formation with upregulated expression of cytochrome p450-1a1 gene[J]. Experimental hematology,2007,35(8):1249-1255. |
APA | Xu, Min,Li, Dao,Lu, Ying,&Chen, Guo-Qiang.(2007).Leukemogenic aml1-eto fusion protein increases carcinogen-dna adduct formation with upregulated expression of cytochrome p450-1a1 gene.Experimental hematology,35(8),1249-1255. |
MLA | Xu, Min,et al."Leukemogenic aml1-eto fusion protein increases carcinogen-dna adduct formation with upregulated expression of cytochrome p450-1a1 gene".Experimental hematology 35.8(2007):1249-1255. |
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来源:中国科学院大学
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