MicroRNA-205 functions as a tumor suppressor in colorectal cancer by targeting cAMP responsive element binding protein 1 (CREB1)

MicroRNAs (miRNA) have been documented playing critical roles in cancer progression. Aberrant expression of miR-205 has been reported in several types of cancer. However, the role and mechanism of miR-205 in colorectal cancer (CRC) remains unclear. In this study, the expression levels of miR-205 in...

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Published inAmerican journal of translational research Vol. 7; no. 10; pp. 2053 - 2059
Main Authors Li, Peng, Xue, Wan-Jiang, Feng, Ying, Mao, Qin-Sheng
Format Journal Article
LanguageEnglish
Published United States e-Century Publishing Corporation 01.01.2015
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Summary:MicroRNAs (miRNA) have been documented playing critical roles in cancer progression. Aberrant expression of miR-205 has been reported in several types of cancer. However, the role and mechanism of miR-205 in colorectal cancer (CRC) remains unclear. In this study, the expression levels of miR-205 in CRC tissues and cell lines were detected by quantitative real-time PCR (qRT-PCR). MTT assay and transwell assays were applied to assess the effect of miR-205 on CRC cell proliferation, migration and invasion abilities in vitro. Furthermore, Dual-luciferase reporter assay was conducted to confirm the direct binding of miR-205 and target genes. In the present study, we found that the expression level of miR-205 in CRC tissues and cell lines was significantly down-regulated. Functional assays showed that overexpression of miR-205 suppressed CRC cell proliferation, migration and invasion in vitro. In addition, cAMP responsive element binding protein 1 (CREB1) was identified as targets of miR-205. Silencing CREB1 had similar effects of miR-205 restoration on proliferation, migration and invasion in CRC cells. Our results demonstrated that miR-205 may act as a tumor suppressor by targeting the CREB1 gene and suppressing CRC cell proliferation, migration and invasion. Thus, miR-205 may represent a potential therapeutic target for CRC intervention.
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ISSN:1943-8141
1943-8141