Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 안영호 | * |
dc.date.accessioned | 2016-08-27T04:08:15Z | - |
dc.date.available | 2016-08-27T04:08:15Z | - |
dc.date.issued | 2015 | * |
dc.identifier.issn | 0021-9738 | * |
dc.identifier.issn | 1558-8238 | * |
dc.identifier.other | OAK-14644 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/217059 | - |
dc.description.abstract | Epithelial tumor metastasis is preceded by an accumulation of collagen cross-links that heighten stromal stiffness and stimulate the invasive properties of tumor cells. However, the biochemical nature of collagen cross-links in cancer is still unclear. Here, we postulated that epithelial tumorigenesis is accompanied by changes in the biochemical type of collagen cross-links. Utilizing resected human lung cancer tissues and a p21(CIP1/WAF1)-deficient, K-ras(G12D)-expressing murine metastatic lung cancer model, we showed that, relative to normal lung tissues, tumor stroma contains higher levels of hydroxylysine aldehyde-derived collagen cross-links (HLCCs) and lower levels of lysine aldehyde-derived cross-links (LCCs), which are the predominant types of collagen cross-links in skeletal tissues and soft tissues, respectively. Gain- and loss-of-function studies in tumor cells showed that lysyl hydroxylase 2 (LH2), which hydroxylates telopeptidyl lysine residues on collagen, shifted the tumor stroma toward a high-HLCC, low-LCC state, increased tumor stiffness, and enhanced tumor cell invasion and metastasis. Together, our data indicate that LH2 enhances the metastatic properties of tumor cells and functions as a regulatory switch that controls the relative abundance of biochemically distinct types of collagen cross-links in the tumor stroma. | * |
dc.language | English | * |
dc.publisher | AMER SOC CLINICAL INVESTIGATION INC | * |
dc.title | Lysyl hydroxylase 2 induces a collagen cross-link switch in tumor stroma | * |
dc.type | Article | * |
dc.relation.issue | 3 | * |
dc.relation.volume | 125 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 1147 | * |
dc.relation.lastpage | 1162 | * |
dc.relation.journaltitle | JOURNAL OF CLINICAL INVESTIGATION | * |
dc.identifier.doi | 10.1172/JCI74725 | * |
dc.identifier.wosid | WOS:000350616500029 | * |
dc.author.google | Chen, Yulong | * |
dc.author.google | Terajima, Masahiko | * |
dc.author.google | Yang, Yanan | * |
dc.author.google | Sun, Li | * |
dc.author.google | Ahn, Young-Ho | * |
dc.author.google | Pankova, Daniela | * |
dc.author.google | Puperi, Daniel S. | * |
dc.author.google | Watanabe, Takeshi | * |
dc.author.google | Kim, Min P. | * |
dc.author.google | Blackmon, Shanda H. | * |
dc.author.google | Rodriguez, Jaime | * |
dc.author.google | Liu, Hui | * |
dc.author.google | Behrens, Carmen | * |
dc.author.google | Wistuba, Ignacio I. | * |
dc.author.google | Minelli, Rosalba | * |
dc.author.google | Scott, Kenneth L. | * |
dc.author.google | Sanchez-Adams, Johannah | * |
dc.author.google | Guilak, Farshid | * |
dc.author.google | Pati, Debananda | * |
dc.author.google | Thilaganathan, Nishan | * |
dc.author.google | Burns, Alan R. | * |
dc.author.google | Creighton, Chad J. | * |
dc.author.google | Martinez, Elisabeth D. | * |
dc.author.google | Zal, Tomasz | * |
dc.author.google | Grande-Allen, K. Jane | * |
dc.author.google | Yamauchi, Mitsuo | * |
dc.author.google | Kurie, Jonathan M. | * |
dc.contributor.scopusid | 안영호(7202402440) | * |
dc.date.modifydate | 20240222132209 | * |