[No authors listed]
Colon cancer is one of the most frequent malignant tumors, and microRNA (miR)â205 is involved in the tumor progression. The present study aimed to explore the effects of miRâ205 on human colon cancer and its targeting mechanism. The levels of miRâ205 and mouse double minute 4 (MDM4) were determined via reverse transcriptionâquantitative (RTâq)PCR and western blot analysis. A luciferase activity assay was performed to analyze the association between miRâ205 and MDM4. Cell viability, migration and invasion were determined via Cell Counting Kitâ8, wound healing and Transwell assays, respectively. The levels of epithelialâmesenchymal transition (EMT)âassociated factors were determined by RTâqPCR and western blot analysis. It was identified that MDM4 was overexpressed in colon cancer tissues and cells, and that there was a negative correlation between miRâ205 and MDM4 expression in colon cancer. Similarly, miRâ205 inhibited MDM4 expression by binding to its 3'untranslated region. in addition, miRâ205 directly targeted MDM4, accompanied by suppressed proliferation, migration and invasion of HCT116 cells. EMT processes were suppressed in miRâ205âoverexpressed cells; upregulation of Eâcadherin, and downregulation of Nâcadherin, vimentin, matrix metalloproteinase (MMP)2 and MMP9 were observed. Collectively, miRâ205 conspicuously depressed the viability, migration, invasion and EMT process of human colon cancer cells via targeting MDM4. miRâ205 could be potentially used in the treatment of human colon cancer.
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