miR-296 inhibits the metastasis and epithelial-mesenchymal transition of colorectal cancer by targeting S100A4Reportar como inadecuado

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BMC Cancer

, 17:140

Cell and molecular biology


BackgroundDysregulation of microRNAs miRNAs is actively involved in the pathogenesis and tumorigenicity of colorectal cancer CRC. miR-296 was found to play either oncogenic or tumor suppressive role in human cancers. However, the status of miR-296 and its function in CRC remain unknown.

MethodsThe expression of miR-296 was confirmed by qRT-PCR in CRC tissues and cells, and its level was altered by corresponding miRNA vectors. Wound healing and Transwall assays were performed to detect the migration and invasion of CRC cells. The levels of proteins were measured using immunoblotting, immunohistochemistry and immunofluorescence.

ResultsUnderexpression of miR-296 was disclosed in CRC tissues and cells. Its decreased level was evidently correlated with adverse clinical parameters and poor prognosis of CRC patients. In vitro experiments indicated that miR-296 inhibited CRC cell migration and invasion. Mechanically, miR-296 inhibited the epithelial-mesenchymal transition EMT of CRC cells. A negative correlation between miR-296 and S100A4 expression was observed in CRC tissues. Luciferase reporter assays indicated that miR-296 inversely regulated the luciferase activity of 3’-UTR of S100A4. Herein, S100A4 was found to be a downstream molecule of miR-296 in CRC. Furthermore, S100A4 mediated the anti-metastatic effects of miR-296 on EMT, migration and invasion of CRC cells.

ConclusionsmiR-296 functions as an anti-metastatic factor mainly by suppressing S100A4 in CRC. It potentially acts as a prognostic predictor and a drug-target for CRC patients.

KeywordsmiR-296 Colorectal cancer Metastasis Epithelial-mesenchymal transition S100A4 AbbreviationsCRCColorectal cancer

EMTEpithelial-mesenchymal transition




qRT-PCRQuantitative real-time polymerase chain reaction


Electronic supplementary materialThe online version of this article doi:10.1186-s12885-017-3121-z contains supplementary material, which is available to authorized users.

Autor: Zheng He - Lianhua Yu - Shiyi Luo - Mingzhen Li - Junbo Li - Qi Li - Yi Sun - Chengbin Wang

Fuente: https://link.springer.com/

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