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学科主题临床医学
BMPR2 inhibition induced apoptosis and autophagy via destabilization of XIAP in human chondrosarcoma cells
Jiao, G.1; Guo, W.1; Ren, T.1; Lu, Q.1; Sun, Y.1; Liang, W.1; Ren, C.1; Yang, K.1; Sun, K.2
刊名CELL DEATH & DISEASE
2014-12-01
DOI10.1038/cddis.2014.540
5
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Cell Biology
研究领域[WOS]Cell Biology
关键词[WOS]MORPHOGENETIC PROTEIN-RECEPTOR ; PROSTATE-CANCER CELLS ; X-LINKED INHIBITOR ; BONE ; EXPRESSION ; GROWTH ; FAMILY ; GENES ; DEATH ; DEGRADATION
英文摘要

Bone morphogenetic proteins (BMPs) are multifunctional proteins, and their receptors (BMPRs) have crucial roles in the process of signaling. However, their function in cancer is somewhat inconsistent. It has been demonstrated that more prevalent expression of bone morphogenetic protein receptor 2 (BMPR2) has been detected in dedifferentiated chondrosarcomas than conventional chondrosarcomas. Here, we find that BMPR2 inhibition induces apoptosis and autophagy of chondrosarcoma. We found that BMPR2 expression was correlated with the clinicopathological features of chondrosarcomas, and could predict the treatment outcome. Knockdown of BMPR2 by small interfering RNA results in growth inhibition in chondrosarcoma cells. Silencing BMPR2 promoted G2/M cell cycle arrest, induced chondrosarcoma cell apoptosis through caspase-3-dependent pathway via repression of X-linked inhibitor of apoptosis protein (XIAP) and induced autophagy of chondrosarcoma cells via XIAP-Mdm2-p53 pathway. Inhibition of autophagy induced by BMPR2 small interfering RNA (siBMPR2) sensitized chondrosarcoma cells to siBMPR2-induced apoptotic cell death, suggesting that autophagy has a protective role for chondrosarcoma cells in context of siBMPR2-induced apoptotic cell death. In vivo tumorigenicity assay in mice indicated that inhibition of BMPR2 reduced tumor growth. Taken together, our results suggest that BMPR2 has a significant role in the tumorigenesis of chondrosarcoma, and could be an important prognostic marker for chondrosarcoma. BMPR2 inhibition could eventually provide a promising therapy for chondrosarcoma treatment.

语种英语
WOS记录号WOS:000347837400024
项目编号81172543 ; 20130001110076
资助机构Natural Science Foundation of China ; Specialised Research Fund for the Doctoral Programme of Higher Education of China
引用统计
被引频次:15[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/400002259/60837
专题北京大学第二临床医学院_骨肿瘤科
北京大学药学院_天然药物与仿生药物国家重点实验室
北京大学第二临床医学院_医疗美容科
北京大学公共卫生学院_学院办公室
作者单位1.Peking Univ, Peoples Hosp, Musculoskeletal Tumor Ctr, Beijing 100044, Peoples R China
2.Peking Univ, Peoples Hosp, Dept Pathol, Beijing 100044, Peoples R China
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GB/T 7714
Jiao, G.,Guo, W.,Ren, T.,et al. BMPR2 inhibition induced apoptosis and autophagy via destabilization of XIAP in human chondrosarcoma cells[J]. CELL DEATH & DISEASE,2014,5.
APA Jiao, G..,Guo, W..,Ren, T..,Lu, Q..,Sun, Y..,...&Sun, K..(2014).BMPR2 inhibition induced apoptosis and autophagy via destabilization of XIAP in human chondrosarcoma cells.CELL DEATH & DISEASE,5.
MLA Jiao, G.,et al."BMPR2 inhibition induced apoptosis and autophagy via destabilization of XIAP in human chondrosarcoma cells".CELL DEATH & DISEASE 5(2014).
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