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学科主题临床医学
Silencing HCCR2 expression inhibits the proliferation of leukemia cells by inducing apoptosis and promoting cell cycle arrest
Qiao, Shu-Kai; Ren, Han-Yun; Shi, Yong-Jin; Liu, Wei
关键词human cervical cancer oncogene small interfering RNA apoptosis cell cycle acute leukemia
刊名INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
2013-12-01
DOI10.3892/ijmm.2013.1518
32期:6页:1373-1379
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Medicine, Research & Experimental
研究领域[WOS]Research & Experimental Medicine
关键词[WOS]ACUTE MYELOID-LEUKEMIA ; ACUTE LYMPHOBLASTIC-LEUKEMIA ; GENE-SPECIFIC THERAPEUTICS ; BREAST-CANCER ; RNA INTERFERENCE ; HEPATOCELLULAR-CARCINOMA ; P53 STABILIZATION ; ONCOGENE HCCR-2 ; TUMORIGENESIS ; TRANSPLANTATION
英文摘要

The human cervical cancer oncogene (HCCR2) has been found to be overexpressed in a variety of human malignant tumors cells, and its function is related to cell cycle progression and survival. However, the molecular mechanisms of action of HCCR2 in leukemia remain unclear. In this study, we used the RNA interference strategy to investigate the effects of HCCR2 knockdown in the K562 leukemia cell line, and to explore the potential mechanisms involved. Following transfection with small interfering RNA (siRNA) targeting HCCR2 (HCCR2-siRNA), we examined the effects of HCCR2 knockdown on cell morphology, cell proliferation, cell cycle progression and apoptosis in K562 cells. Morphological changes were evaluated by Wright-Giemsa staining. Cell cycle progression and apoptosis were measured by flow cytometry. The expression levels of genes related to the cell cycle and apoptosis were detected by quantitative RT-PCR (qRT-PCR) and western blot analysis. HCCR2 expression at the mRNA and protein level was significantly decreased following transfection with plasmids expressing HCCR2-siRNA. Silencing HCCR2 expression significantly suppressed cell proliferation, induced G1 cell cycle arrest and promoted the apoptosis of K562 cells. Additionally, we found that the expression of Bax, p53 and p21 was significantly increased, while Bcl-2 expression was significantly decreased in the HCCR2-siRNA-transfected cells. However, the expression of p27 was not affected. These results suggest that the HCCR2 gene plays an important role in the tumorigenesis of leukemia, thus making it an attractive therapeutic target for acute leukemia.

语种英语
WOS记录号WOS:000330225300018
引用统计
被引频次:3[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/62533
专题北京大学第一临床医学院_血液内科
作者单位Peking Univ First Hosp, Dept Hematol, Beijing 100034, Peoples R China
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Qiao, Shu-Kai,Ren, Han-Yun,Shi, Yong-Jin,et al. Silencing HCCR2 expression inhibits the proliferation of leukemia cells by inducing apoptosis and promoting cell cycle arrest[J]. INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE,2013,32(6):1373-1379.
APA Qiao, Shu-Kai,Ren, Han-Yun,Shi, Yong-Jin,&Liu, Wei.(2013).Silencing HCCR2 expression inhibits the proliferation of leukemia cells by inducing apoptosis and promoting cell cycle arrest.INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE,32(6),1373-1379.
MLA Qiao, Shu-Kai,et al."Silencing HCCR2 expression inhibits the proliferation of leukemia cells by inducing apoptosis and promoting cell cycle arrest".INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE 32.6(2013):1373-1379.
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