Cargando…
miR-582-5P induces colorectal cancer cell proliferation by targeting adenomatous polyposis coli
BACKGROUND: microRNA (miRNAs) dysregulation is widely involved in cancer progression and contributed to sustained cell proliferation by directly targeting multiple targets. Therefore, better understand the underlying mechanism of miRNA in carcinogenesis may improve diagnostic and therapeutic strateg...
Autores principales: | , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2016
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5011851/ https://www.ncbi.nlm.nih.gov/pubmed/27595705 http://dx.doi.org/10.1186/s12957-016-0984-4 |
Sumario: | BACKGROUND: microRNA (miRNAs) dysregulation is widely involved in cancer progression and contributed to sustained cell proliferation by directly targeting multiple targets. Therefore, better understand the underlying mechanism of miRNA in carcinogenesis may improve diagnostic and therapeutic strategies for malignancy. METHODS: We assessed microRNA-582 (miR-582-5P) expression in colorectal cancer (CRC) specimens and cell lines by real-time PCR. Luciferase reporter assay was used to confirm the target associations. Colony formation assay and anchorage-independent growth assay were used to analyze the effect of miR-582-5P on cell proliferation. Adenomatous polyposis coli (APC) gene and protein expression were examined using real-time PCR and western blotting, respectively. RESULTS: miR-582-5P was upregulated in the CRC specimens and cell lines and targeted the 3′ untranslated region of APC directly. miR-582-5P overexpression increased cyclin D1 and c-MYC expression, which subsequently induced CRC cell proliferation in an APC-dependent manner. CONCLUSIONS: Our findings suggest that miR-582-5P plays an important role in the progression of CRC by inducing proliferation and may identify new targets for anti-cancer treatment. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12957-016-0984-4) contains supplementary material, which is available to authorized users. |
---|