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dc.contributor.authorChen, Hsin-Yien_US
dc.contributor.authorLin, Yu-Minen_US
dc.contributor.authorChung, Hsiang-Chingen_US
dc.contributor.authorLang, Yaw-Dongen_US
dc.contributor.authorLin, Ching-Jungen_US
dc.contributor.authorHuang, Johnen_US
dc.contributor.authorWang, Wei-Chien_US
dc.contributor.authorLin, Feng-Maoen_US
dc.contributor.authorChen, Zhenen_US
dc.contributor.authorHuang, Hsien-Daen_US
dc.contributor.authorShyy, John Y. -J.en_US
dc.contributor.authorLiang, Jin-Tungen_US
dc.contributor.authorChen, Ruey-Hwaen_US
dc.date.accessioned2014-12-08T15:24:25Z-
dc.date.available2014-12-08T15:24:25Z-
dc.date.issued2012-07-15en_US
dc.identifier.issn0008-5472en_US
dc.identifier.urihttp://dx.doi.org/10.1158/0008-5472.CAN-12-0667en_US
dc.identifier.urihttp://hdl.handle.net/11536/16939-
dc.description.abstractMetastasis is the major cause of poor prognosis in colorectal cancer (CRC), and increasing evidence supports the contribution of miRNAs to cancer progression. Here, we found that high expression of miR-103 and miR-107 (miR-103/107) was associated with metastasis potential of CRC cell lines and poor prognosis in patients with CRC. We showed that miR-103/107 targeted the known metastasis suppressors death-associated protein kinase (DAPK) and Kruppel-like factor 4 (KLF4) in CRC cells, resulting in increased cell motility and cell-matrix adhesion and decreased cell-cell adhesion and epithelial marker expression. miR-103/107 expression was increased in the presence of hypoxia, thereby potentiating DAPK and KLF4 downregulation and hypoxia-induced motility and invasiveness. In mouse models of CRC, miR-103/107 overexpression potentiated local invasion and liver metastasis effects, which were suppressed by reexpression of DAPK or KLF4. miR-103/107-mediated downregulation of DAPK and KLF4 also enabled the colonization of CRC cells at a metastatic site. Clinically, the signature of a miR-103/107 high, DAPK low, and KLF4 low expression profile correlated with the extent of lymph node and distant metastasis in patients with CRC and served as a prognostic marker for metastasis recurrence and poor survival. Our findings therefore indicate that miR-103/107-mediated repression of DAPK and KLF4 promotes metastasis in CRC, and this regulatory circuit may contribute in part to hypoxia-stimulated tumormetastasis. Strategies that disrupt this regulation might be developed to block CRC metastasis. Cancer Res; 72(14); 3631-41. (c) 2012 AACR.en_US
dc.language.isoen_USen_US
dc.titlemiR-103/107 Promote Metastasis of Colorectal Cancer by Targeting the Metastasis Suppressors DAPK and KLF4en_US
dc.typeArticleen_US
dc.identifier.doi10.1158/0008-5472.CAN-12-0667en_US
dc.identifier.journalCANCER RESEARCHen_US
dc.citation.volume72en_US
dc.citation.issue14en_US
dc.citation.spage3631en_US
dc.citation.epage3641en_US
dc.contributor.department生物資訊及系統生物研究所zh_TW
dc.contributor.departmentInstitude of Bioinformatics and Systems Biologyen_US
dc.identifier.wosnumberWOS:000307353200020-
dc.citation.woscount71-
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