题名 | Pure curcumin decreases the expression of WT1 by upregulation of miR-15a and miR-16-1 in leukemic cells |
作者 | |
发表日期 | 2012-03-27 |
发表期刊 | JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH 影响因子和分区 |
语种 | 英语 |
原始文献类型 | Article |
关键词 | Curcumin WT1 miR-15a miR-16-1 |
其他关键词 | MINIMAL RESIDUAL DISEASE ; GENE-EXPRESSION ; MICRORNAS ; PROLIFERATION ; SUPPRESSOR ; TARGET ; TOOL ; PCR |
摘要 | Background: Pure curcumin has been reported to down-regulate the expression of WT1 in leukemic cells. However, the molecular mechanism underlying the down-regulation of WT1 by curcumin is not completely delineated. The purpose of this present study is to identify a new miRNA-mediated mechanism which plays an important role in the anti-proliferation effects of curcumin in leukemic cells. Methods: K562 and HL-60 cells were treated with different concentrations of curcumin for 24 and 48 hours, the level of miR-15a/16-1 and WT1 were detected by qRT-PCR and Western blotting. WT1 expression and cell proliferation were detected by Western blotting and CCK-8, after curcumin treated-K562 and HL-60 cells were transfected with anti-miR-15a/16-1 oligonucleotides. Results: We found that pure curcumin upregulated the expression of miR-15a/16-1 and downregulated the expression of WT1 in leukemic cells and primary acute myeloid leukemia (AML) cells. Overexpression of miR-15a/16-1 deduced the protein level of WT1 in leukemic cells, but downregulation of WT1 by siRNA-WT1 could not increase the expression of miR-15a/16-1 in leukemic cells. These results reveal that curcumin induced-upregulation of miR-15a/16-1 is an early event upstream to downregulation of WT1. Furthermore, anti-miR-15a/16-1 oligonucleotides (AMO) partly reversed the downregulation of WT1 induced by pure curcumin in leukemic cells and AMO promoted the growth of curcumin treated-K562 and HL-60 cells. Conclusion: Thus, these data suggest for the first time that pure curcumin downregulated the expression of WT1 partly by upregulating the expression of miR-15a/16-1 in leukemic cells. miR-15a/16-1 mediated WT1 downregulation plays an important role in the anti-proliferation effect of curcumin in leukemic cells. |
资助项目 | National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [81172613]; Zhejiang Provincial Natural Science Foundation of ChinaNatural Science Foundation of Zhejiang Province [Y2101069, Y206383, Y12H080019]; Scientifical Research Foundation of Zhejiang Provincial Education Department [Y201119952] |
出版者 | BMC |
出版地 | LONDON |
ISSN | 1756-9966 |
EISSN | 1756-9966 |
卷号 | 31期号:1页码:27 |
DOI | 10.1186/1756-9966-31-27 |
页数 | 9 |
WOS类目 | Oncology |
WOS研究方向 | Oncology |
WOS记录号 | WOS:000302803500001 |
收录类别 | SCIE ; PUBMED |
URL | 查看原文 |
PubMed ID | 22449094 |
PMC记录号 | PMC3325897 |
通讯作者地址 | [Yu, Kang]Wenzhou Med Coll, Affiliated Hosp 1, Dept Hematol, 2 FuXue Rd, Wenzhou 325000, Peoples R China. |
TOP期刊 | TOP期刊 |
引用统计 | |
文献类型 | 期刊论文 |
条目标识符 | https://kms.wmu.edu.cn/handle/3ETUA0LF/19229 |
专题 | 附属第一医院 附属第二医院 第二临床医学院,附属第二医院、育英儿童医院 附属第二医院_药物临床试验办公室 |
通讯作者 | Yu, Kang |
作者单位 | 1.Wenzhou Med Coll, Affiliated Hosp 1, Dept Hematol, Wenzhou 325000, Peoples R China; 2.Wenzhou Med Coll, Affiliated Hosp 1, Lab Internal Med, Wenzhou 325000, Peoples R China; 3.Wenzhou Med Coll, Affiliated Hosp 2, Clin Lab, Wenzhou 325000, Peoples R China |
第一作者单位 | 附属第一医院 |
通讯作者单位 | 附属第一医院 |
第一作者的第一单位 | 附属第一医院 |
推荐引用方式 GB/T 7714 | Gao, Shen-meng,Yang, Jun-jun,Chen, Chi-qi,et al. Pure curcumin decreases the expression of WT1 by upregulation of miR-15a and miR-16-1 in leukemic cells[J]. JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH,2012,31(1):27. |
APA | Gao, Shen-meng., Yang, Jun-jun., Chen, Chi-qi., Chen, Jun-jie., Ye, Li-ping., ... & Yu, Kang. (2012). Pure curcumin decreases the expression of WT1 by upregulation of miR-15a and miR-16-1 in leukemic cells. JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH, 31(1), 27. |
MLA | Gao, Shen-meng,et al."Pure curcumin decreases the expression of WT1 by upregulation of miR-15a and miR-16-1 in leukemic cells".JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH 31.1(2012):27. |
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