Journal
MOLECULAR AND CELLULAR BIOCHEMISTRY
Volume 393, Issue 1-2, Pages 283-291Publisher
SPRINGER
DOI: 10.1007/s11010-014-2071-x
Keywords
Epithelial-mesenchymal transition; Glioma-associated oncogene homolog-1; Hepatocellular carcinoma; Invasion; Matrix metalloproteinase
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Funding
- National Natural Science Foundation of China [81201930, 81101862, 81172079]
- Research Fund for the Doctoral Program of Higher Education of China [20124423120006]
- Natural Science Foundation of Guangdong Province [S2012040006803, S2013010016831]
- Key Project of Guangzhou Municipal Science & Technology Planning [2011J4100053]
- Doctoral Research Foundation of Guangzhou Medical University [2010C23]
- Foundation for Youth Teachers by Sun Yat-Sen University [11ykpy16]
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Glioma-associated oncogene homolog-1 (Gli-1) is considered a marker of Hedgehog pathway activation and is associated with the progression of several cancers. We have previously reported that Gli-1 was correlated with invasion and metastasis in hepatocellular carcinoma (HCC). However, the exact roles and mechanisms of Gli-1 in HCC invasion are unclear. In this study, we found that small interfering RNA mediated down-regulation of Gli-1 expression significantly suppressed adhesion, motility, migration, and invasion of both SMMC-7721 and SK-Hep1 cells. Furthermore, down-regulation of Gli-1 significantly reduced expressions and activities of both matrix metalloproteinase (MMP)-2 and MMP-9. In addition, we found that down-regulation of Gli-1 resulted in up-regulation of E-cadherin and concomitant down-regulation of Snail and Vimentin, consistent with inhibition of epithelial-mesenchymal transition (EMT). Taken together, our results suggest that down-regulation of Gli-1 suppresses HCC cell migration and invasion likely through inhibiting expressions and activations of MMP-2, 9 and blocking EMT.
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