JNK signaling maintains the mesenchymal properties of multi-drug resistant human epidermoid carcinoma KB cells through snail and twist1
文献类型:期刊论文
作者 | Zhan, Xia4; Feng, Xiaobing1,3,4; Kong, Ying4; Chen, Yi2![]() |
刊名 | BMC CANCER
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出版日期 | 2013-04-04 |
卷号 | 13 |
关键词 | c-Jun N-terminal kinases Snail Twist1 Epithelial mesenchymal transition |
ISSN号 | 1471-2407 |
DOI | 10.1186/1471-2407-13-180 |
文献子类 | Article |
英文摘要 | Background and methods: In addition to possess cross drug resistance characteristic, emerging evidences have shown that multiple-drug resistance (MDR) cancer cells exhibit aberrant metastatic capacity when compared to parental cells. In this study, we explored the contribution of c-Jun N-terminal kinases (JNK) signaling to the mesenchymal phenotypes and the aberrant motile capacity of MDR cells utilizing a well characterized MDR cell line KB/VCR, which is established from KB human epidermoid carcinoma cells by vincristine (VCR), and its parental cell line KB. Results: Taking advantage of experimental strategies including pharmacological tool and gene knockdown, we showed here that interference with JNK signaling pathway by targeting JNK1/2 or c-Jun reversed the mesenchymal properties of KB/VCR cells to epithelial phenotypes and suppressed the motile capacity of KB/VCR cells, such as migration and invasion. These observations support a critical role of JNK signaling in maintaining the mesenchymal properties of KB/VCR cells. Furthermore, we observed that JNK signaling may control the expression of both snail and twist1 in KB/VCR cells, indicating that both snail and twist1 are involved in controlling the mesenchymal characteristics of KB/VCR cells by JNK signaling. Conclusion: JNK signaling is required for maintaining the mesenchymal phenotype of KB/VCR cells; and JNK signaling may maintain the mesenchymal characteristics of KB/VCR cells potentially through snail and twist1. |
WOS关键词 | JUN NH2-TERMINAL KINASE ; BREAST-CANCER CELLS ; N-TERMINAL KINASE ; DRUG-RESISTANCE ; C-JUN ; STEM-CELLS ; HEPATOCELLULAR-CARCINOMA ; ACTIVATION ; TRANSITION ; METASTASIS |
资助项目 | National Natural Science Foundation of China[81173077] ; "Interdisciplinary Cooperation Team" Program for Science and Technology Innovation of the Chinese Academy of Sciences[00000000] |
WOS研究方向 | Oncology |
语种 | 英语 |
WOS记录号 | WOS:000318493300001 |
出版者 | BIOMED CENTRAL LTD |
源URL | [http://119.78.100.183/handle/2S10ELR8/277662] ![]() |
专题 | 药理学第一研究室 中科院受体结构与功能重点实验室 新药研究国家重点实验室 |
通讯作者 | Chen, Yi |
作者单位 | 1.Peking Univ, Beijing Canc Hosp, Sch Oncol, Dept Integrat Tradit Chinese & Western Med, Beijing 100871, Peoples R China 2.Chinese Acad Sci, Shanghai Inst Mat Med, State Key Lab Drug Res, Shanghai 201203, Peoples R China; 3.Nantong Univ, Sch Med, Nantong 226001, Peoples R China; 4.Fudan Univ, Sch Pharm, Dept Pharmacol, Shanghai 201203, Peoples R China; |
推荐引用方式 GB/T 7714 | Zhan, Xia,Feng, Xiaobing,Kong, Ying,et al. JNK signaling maintains the mesenchymal properties of multi-drug resistant human epidermoid carcinoma KB cells through snail and twist1[J]. BMC CANCER,2013,13. |
APA | Zhan, Xia,Feng, Xiaobing,Kong, Ying,Chen, Yi,&Tan, Wenfu.(2013).JNK signaling maintains the mesenchymal properties of multi-drug resistant human epidermoid carcinoma KB cells through snail and twist1.BMC CANCER,13. |
MLA | Zhan, Xia,et al."JNK signaling maintains the mesenchymal properties of multi-drug resistant human epidermoid carcinoma KB cells through snail and twist1".BMC CANCER 13(2013). |
入库方式: OAI收割
来源:上海药物研究所
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