Abstract
Metastasis is the main cause of mortality in patients with solid tumours. Identifying the exact molecules associated with CRC metastasis may be crucial to understand the process, which might also be translated to the diagnosis and treatment of CRC. In this study, we investigate the association of microRNA expression patterns with the lymph node metastasis of colorectal cancer. Among these candidate miRNAs, the expression of miRNA-145 was significantly related to lymph node metastasis of CRC. Both in vitro and in vivo study demonstrated that up-regulation of miR-145 could improve the ability of migration and invasion of colorectal cancer cell, while no effect on proliferation was observed. The mechanism of this promotion is associated with the stabilization of Hsp-27, a protein which plays an important role in the promotion of metastasis. These results may be crucial to understanding CRC metastasis and may be translated to the diagnosis and treatment of CRC.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Biomarkers, Tumor / metabolism
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Cell Movement / drug effects
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Colorectal Neoplasms / physiopathology*
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Gene Expression Profiling
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Gene Expression Regulation, Neoplastic / physiology*
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HSP27 Heat-Shock Proteins / metabolism
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Heat-Shock Proteins
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Humans
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Lymphatic Metastasis / physiopathology*
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MicroRNAs / metabolism*
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MicroRNAs / pharmacology
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Molecular Chaperones
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Neoplasm Invasiveness / physiopathology
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Real-Time Polymerase Chain Reaction
Substances
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Biomarkers, Tumor
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HSP27 Heat-Shock Proteins
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HSPB1 protein, human
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Heat-Shock Proteins
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MIRN145 microRNA, human
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MicroRNAs
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Molecular Chaperones
Grants and funding
This study was supported by the National Basic Research Program of China (Grant no. 2011CB911004), The Beijing Training Project for The Leading Talents (Z131107000513001), Beijing Nova Program (Z131107000413066) and Beijing Natural Science Foundation of China (Grant no. 7122150). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.