MicroRNA-223 functions as an oncogene in human colorectal cancer cells
Aberrant microRNA (miRNA) expression has been frequently observed in colorectal cancer (CRC), the third most common human cancer in the world. However, the roles of miRNAs in CRC remain poorly understood. The present study explored, identified and characterized the miRNAs that correlate with CRC pro...
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Published in | Oncology reports Vol. 32; no. 1; pp. 115 - 120 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
Greece
D.A. Spandidos
01.07.2014
Spandidos Publications Spandidos Publications UK Ltd |
Subjects | |
Online Access | Get full text |
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Summary: | Aberrant microRNA (miRNA) expression has been frequently observed in colorectal cancer (CRC), the third most common human cancer in the world. However, the roles of miRNAs in CRC remain poorly understood. The present study explored, identified and characterized the miRNAs that correlate with CRC progression. Deregulated level of microRNA-223 (miR-223) was screened out by miRNA microarray in colorectal tumor tissues and further confirmed by quantitative real-time PCR in a large cohort of CRC samples (n=90). After silencing miR-223 by artificial anti-miR-223 (miR-223-inhibitor), WST-1 and colony formation assays were employed to assess cell proliferation, and cell migration and invasion were evaluated by wound healing test and Transwell assays, respectively. Compared with adjacent non-tumor tissues, 22 miRNAs were screened out in CRC tissues with significance (>2-fold), of which 13 were upregulated and 9 were downregulated. miR-223 is one of the noticeably upregulated miRNAs. Large cohort CRC sample analyses showed that a higher level of miR-223 correlated with a higher clinical stage. Reducing miR-223 expression resulted in a decreased cell proliferation, migration and invasion in CRC cells. miR-223 functions as an oncomiR in CRC, therefore serving as a potential diagnostic and therapeutic target for the treatment of CRC. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1021-335X 1791-2431 |
DOI: | 10.3892/or.2014.3173 |