Minor Type IV Collagen alpha 5 Chain Promotes Cancer Progression through Discoidin Domain Receptor-1
文献类型：期刊论文
| 作者 | Xiao, Q; Jiang, Y; Liu, QB; Yue, J; Liu, CY; Zhao, XT; Qiao, YM; Ji, HB; Chen, JF; Ge, GX |
| 刊名 | PLOS GENETICS
 |
| 出版日期 | 2015 |
| 卷号 | 11期号:5页码:e0126492-e0126492 |
| 通讯作者 | Xiao, Q (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Biochem & Cell Biol, Key Lab Syst Biol,Innovat Ctr Cell Signaling Netw, Shanghai, Peoples R China.,gxge@sibcb.ac.cn |
| 英文摘要 | Type IV collagens (Col IV), components of basement membrane, are essential in the maintenance of tissue integrity and proper function. Alteration of Col IV is related to developmental defects and diseases, including cancer. Col IV a chains form alpha 1 alpha 1 alpha 2, alpha 3 alpha 4 alpha 5 and alpha 5 alpha 5 alpha 6 protomers that further form collagen networks. Despite knowledge on the functions of major Col IV (alpha 1 alpha 1 alpha 2), little is known whether minor Col IV (alpha 3 alpha 4 alpha 5 and alpha 5 alpha 5 alpha 6) plays a role in cancer. It also remains to be elucidated whether major and minor Col IV are functionally redundant. We show that minor Col IV alpha 5 chain is indispensable in cancer development by using alpha 5(IV)-deficient mouse model. Ablation of alpha 5(IV) significantly impeded the development of Kras(G12D)-driven lung cancer without affecting major Col IV expression. Epithelial alpha 5(IV) supports cancer cell proliferation, while endothelial alpha 5(IV) is essential for efficient tumor angiogenesis. alpha 5(IV), but not alpha 1(IV), ablation impaired expression of non-integrin collagen receptor discoidin domain receptor-1 (DDR1) and downstream ERK activation in lung cancer cells and endothelial cells. Knockdown of DDR1 in lung cancer cells and endothelial cells phenocopied the cells deficient of alpha 5(IV). Constitutively active DDR1 or MEK1 rescued the defects of alpha 5(IV)-ablated cells. Thus, minor Col IV alpha 5(IV) chain supports lung cancer progression via DDR1-mediated cancer cell autonomous and non-autonomous mechanisms. Minor Col IV can not be functionally compensated by abundant major Col IV. |
| 学科主题 | Genetics & Heredity |
| 类目[WOS] | Genetics & Heredity |
| 关键词[WOS] | LINKED ALPORT-SYNDROME ; LUNG-CANCER ; EXTRACELLULAR-MATRIX ; BASEMENT-MEMBRANES ; TUMOR ANGIOGENESIS ; MOUSE MODEL ; CELLS ; GROWTH ; EXPRESSION ; KNOCKOUT |
| 收录类别 | SCI |
| 语种 | 英语 |
| WOS记录号 | WOS:000355305200056 |
| 版本 | 出版稿 |
| 源URL | [http://202.127.25.143/handle/331003/64]  |
| 专题 | 上海生化细胞研究所_上海生科院生化细胞研究所 |
| 推荐引用方式 GB/T 7714 | Xiao, Q,Jiang, Y,Liu, QB,et al. Minor Type IV Collagen alpha 5 Chain Promotes Cancer Progression through Discoidin Domain Receptor-1[J]. PLOS GENETICS,2015,11(5):e0126492-e0126492. |
| APA | Xiao, Q.,Jiang, Y.,Liu, QB.,Yue, J.,Liu, CY.,...&Ge, GX.(2015).Minor Type IV Collagen alpha 5 Chain Promotes Cancer Progression through Discoidin Domain Receptor-1.PLOS GENETICS,11(5),e0126492-e0126492. |
| MLA | Xiao, Q,et al."Minor Type IV Collagen alpha 5 Chain Promotes Cancer Progression through Discoidin Domain Receptor-1".PLOS GENETICS 11.5(2015):e0126492-e0126492. |
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