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MicroRNA-9 reduces cell invasion and E-cadherin secretion in SK-Hep-1 cell

MicroRNAs (miRNAs) are an abundant class of short noncoding RNAs that can posttranscriptionally regulate gene expression in animals. They are also involved in cancer initiation and progression, and their expression profiles serve as phenotypic signatures of different cancers. The roles played by mic...

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Published in:Medical oncology (Northwood, London, England) London, England), 2010-09, Vol.27 (3), p.654-660
Main Authors: Hao-Xiang, Tan, Qian, Wang, Lian-Zhou, Chen, Xiao-Hui, Huang, Jin-Song, Chen, Xin-Hui, Fu, Liang-Qi, Cao, Xi-Ling, Chen, Wen, Li, Long-juan, Zhang
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Language:English
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Summary:MicroRNAs (miRNAs) are an abundant class of short noncoding RNAs that can posttranscriptionally regulate gene expression in animals. They are also involved in cancer initiation and progression, and their expression profiles serve as phenotypic signatures of different cancers. The roles played by microRNAs specifically in “micromanagement of metastasis” has been addressed only recently. The molecular mechanisms of hepatocellular carcinoma (HCC) metastasis are still poorly understood. Recent evidence implies genetic determinants of cancer metastasis. Because gene expression signature significantly differs between primary metastasis-free HCC and primary HCC with intrahepatic metastases, miRNA expression in those primary HCC may change correspondingly. The 28 up-regulated miRNAs, part of the reported miRNA profiles of HCC, were compared in primary HCC with or without metastases. Only eight miRNAs were found to be significantly up-regulated in primary HCC with metastases while miR-9 had the highest hold change. miR-9 was highly expressed in SK-Hep-1 cell when compared with other hepatoma cell lines and downregulation of miR-9 reduced SK-Hep-1 cell invasion. E-cadherin, a tumor invasion suppressor in HCC, was found to be a putative gene target of miR-9. E-cadherin was up-regulated by miR-9 inhibitor. The findings suggest miR-9 could be involved in HCC metastasis.
ISSN:1357-0560
1559-131X
DOI:10.1007/s12032-009-9264-2