IR@PKUHSC  > 北京大学第三临床医学院  > 肿瘤放疗科
学科主题临床医学
Bone morphogenetic protein 2 mediates epithelial-mesenchymal transition via AKT and ERK signaling pathways in gastric cancer
Liao, Anyan1; Wang, Weijie2; Sun, Dawei3; Jiang, Yuliang1; Tian, Suqing1; Li, Jinna1; Yang, Xiangshan4; Shi, Ranran5
关键词BMP2 EMT AKT ERK Gastric cancer
刊名TUMOR BIOLOGY
2015-04-01
DOI10.1007/s13277-014-2901-1
36期:4页:2773-2778
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Oncology
研究领域[WOS]Oncology
关键词[WOS]TGF-BETA ; LUNG CARCINOMAS ; TUMOR-GROWTH ; EXPRESSION ; CELLS ; ACTIVATION ; COLON ; EMT
英文摘要

Although deregulation of bone morphogenetic protein 2 (BMP2) signaling has been linked to various types of cancers, the relationships between abnormal activation of these signaling pathways and tumorigenesis are not clear in gastric cancer. We hypothesized that BMP2 might be involved in epithelial-mesenchymal transition (EMT) process of gastric cancer. Here, BMPR-II activation and inhibition in gastric cancer cell line AGS were induced with exogenous BMP2 and with BMPR-II small interfering RNA (siRNA), respectively. BMPR-II downstream signal molecules AKT, ERK phosphorylation, and EMT biomarkers (vimentin, snail, N-cadherin, and E-cadherin) were tested using the Western blot. In the present study, our results showed that BMP2 can induce AKT and ERK phosphorylation in a dose-dependent method, and endogenous BMPR-II can be inhibited completely by BMPR-II siRNA in AGS. Notably BMP2 alone treatment can induce the up-regulation of vimentin, snail, and N-cadherin in AGS cells, besides, the down-regulation of E-cadherin also occurred. On the contrary, BMPR-II siRNA significantly prohibited BMP2-induced AKT and ERK phosphorylation, at the same time, EMT biomarkers changes were not observed. On the other hand, BMPR-II knockdown could significantly affect AGS wound closure and the migration ability (p<0.001) compared to control siRNA and BMP2 alone. In conclusion, this study suggested that EMT process can be triggered by the BMP2/BMPR axis in gastric cancer and then involved in the tumor cell migration, invasion, and metastasis via the activation of PI3K/AKT and MEK/ERK pathways. Our study lays a new foundation for the treatment of gastric cancer through antagonizing BMP2 system.

语种英语
WOS记录号WOS:000352885900063
引用统计
被引频次:19[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/400002259/62693
专题北京大学第三临床医学院_肿瘤放疗科
北京大学第三临床医学院_肿瘤治疗中心
作者单位1.Peking Univ, Dept Radiat Oncol, Hosp 3, Beijing 100191, Peoples R China
2.Shandong Univ, Dept Emergency Surg, Qilu Hosp, Jinan 250100, Shandong, Peoples R China
3.Jilin Univ, Dept Hepatobiliary & Pancreat Surg, Hosp 1, Changchun 130023, Jilin, Peoples R China
4.Shandong Acad Med Sci, Dept Pathol, Affiliated Hosp, Jinan, Shandong, Peoples R China
5.Shandong Univ, Dept Gen Surg, Shandong Prov Hosp Affiliated, Jinan 250100, Shandong, Peoples R China
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GB/T 7714
Liao, Anyan,Wang, Weijie,Sun, Dawei,et al. Bone morphogenetic protein 2 mediates epithelial-mesenchymal transition via AKT and ERK signaling pathways in gastric cancer[J]. TUMOR BIOLOGY,2015,36(4):2773-2778.
APA Liao, Anyan.,Wang, Weijie.,Sun, Dawei.,Jiang, Yuliang.,Tian, Suqing.,...&Shi, Ranran.(2015).Bone morphogenetic protein 2 mediates epithelial-mesenchymal transition via AKT and ERK signaling pathways in gastric cancer.TUMOR BIOLOGY,36(4),2773-2778.
MLA Liao, Anyan,et al."Bone morphogenetic protein 2 mediates epithelial-mesenchymal transition via AKT and ERK signaling pathways in gastric cancer".TUMOR BIOLOGY 36.4(2015):2773-2778.
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