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MicroRNA-222 influences migration and invasion through MIA3 in colorectal cancer

BACKGROUND: miR-222 has been reported to be overexpressed in colorectal cancer and it influences cancer cell proliferation, drug resistance and metastasis. However, the underlying molecular mechanism of miR-222 in colorectal cancer cell invasion and migration has not been thoroughly elucidated to da...

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Detalles Bibliográficos
Autores principales: Gao, Heli, Cong, Xuejing, Zhou, Jianfeng, Guan, Mei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5576312/
https://www.ncbi.nlm.nih.gov/pubmed/28855850
http://dx.doi.org/10.1186/s12935-017-0447-1
Descripción
Sumario:BACKGROUND: miR-222 has been reported to be overexpressed in colorectal cancer and it influences cancer cell proliferation, drug resistance and metastasis. However, the underlying molecular mechanism of miR-222 in colorectal cancer cell invasion and migration has not been thoroughly elucidated to date. METHODS: The cell cycle distribution and apoptosis were assessed by flow cytometry. Cell migration and invasion were analyzed by Transwell assays. The possible target gene of miR-222 was searched and identified by bioinformatics, dual luciferase reporter assay and western blot analysis. The siRNA method was used to confirm the function of the target gene. RESULTS: Overexpression of miR-222 effectively promotes migration and invasion of colorectal cancer (CRC) cells in vitro. Bioinformatics and the dual luciferase reporter assay revealed that miR-222 specifically targeted the 3′-UTR of melanoma inhibitory activity member 3 (MIA3), down-regulating its expression at the protein level. Inhibition of MIA3 by siRNA enhanced the migration and invasion of CRC cell lines. CONCLUSIONS: Our study showed that miR-222 enhances the migration and invasion in CRC cells, primarily by down-regulation of MIA3. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12935-017-0447-1) contains supplementary material, which is available to authorized users.