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  4. Curcumin suppresses metastasis via Sp-1, FAK inhibition, and E-cadherin upregulation in colorectal cancer
 
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Curcumin suppresses metastasis via Sp-1, FAK inhibition, and E-cadherin upregulation in colorectal cancer

Journal
Evidence-based Complementary and Alternative Medicine
Journal Volume
2013
Date Issued
2013
Author(s)
Chen C.-C.
Sureshbabul M.
HUEI-WEN CHEN  
Lin Y.-S.
Lee J.-Y.
Hong Q.-S.
YA-CHIEN YANG  
SUNG-LIANG YU  
DOI
10.1155/2013/541695
URI
https://www.scopus.com/inward/record.uri?eid=2-s2.0-84881535929&doi=10.1155%2f2013%2f541695&partnerID=40&md5=f4a947b20ba9e3d5485650aa7e5703cb
https://scholars.lib.ntu.edu.tw/handle/123456789/596852
Abstract
Colorectal cancer (CRC) is a serious public health problem that results due to changes of diet and various environmental stress factors in the world. Curcumin is a traditional medicine used for treatment of a wide variety of tumors. However, antimetastasis mechanism of curcumin on CRC has not yet been completely investigated. Here, we explored the underlying molecular mechanisms of curcumin on metastasis of CRC cells in vitro and in vivo. Curcumin significantly inhibits cell migration, invasion, and colony formation in vitro and reduces tumor growth and liver metastasis in vivo. We found that curcumin suppresses Sp-1 transcriptional activity and Sp-1 regulated genes including ADEM10, calmodulin, EPHB2, HDAC4, and SEPP1 in CRC cells. Curcumin inhibits focal adhesion kinase (FAK) phosphorylation and enhances the expressions of several extracellular matrix components which play a critical role in invasion and metastasis. Curcumin reduces CD24 expression in a dose-dependent manner in CRC cells. Moreover, E-cadherin expression is upregulated by curcumin and serves as an inhibitor of EMT. These results suggest that curcumin executes its antimetastasis function through downregulation of Sp-1, FAK, and CD24 and by promoting E-cadherin expression in CRC cells. ? 2013 Chun-Chieh Chen et al.
SDGs

[SDGs]SDG3

Other Subjects
calmodulin; CD24 antigen; curcumin; cyclin D3; focal adhesion kinase; gelatinase A; gelatinase B; histone deacetylase 4; pregnancy specific beta1 glycoprotein; protein; protein adem 10; protein ephb2; protein kinase B; protein sepp 1; unclassified drug; uvomorulin; animal experiment; animal model; animal tissue; article; cancer cell culture; cell invasion; cell migration; cell motility; cell proliferation; cell strain HCT116; cell structure; cell viability; colony formation; colorectal cancer; controlled study; dose response; down regulation; drug mechanism; environmental stress; enzyme phosphorylation; gene expression; human; human cell; in vitro study; in vivo study; liver metastasis; mouse; nonhuman; priority journal; protein expression; real time polymerase chain reaction; transcription initiation; tumor growth; upregulation
Type
journal article

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