Human embryonic stem cells and metastatic colorectal cancer cells shared the common endogenous human microRNA-26b

Summary

The increase in proliferation and the lack of differentiation of cancer cells resemble what occur in the embryonic stem cells during physiological process of embryogenesis. There are also striking similarities in the behaviour between the invasive placental cells and invasive cancer cells. In the present study, microarrays were used to analyse the global expression of microRNAs in a human embryonic stem cell line (i.e. HUES-17) and four colorectal cancer (CRC) cell lines (i.e. LoVo, SW480, HT29 and Caco-2) with different metastatic potentialities. Only the expression of miR-26b was significant decreased in HUES-17s and LoVo cells, compared with other three cell lines (P < 0.01). The quantitative real-time PCR analysis confirmed the results of the microarray analysis. Overexpression of miR-26b expression by miR-26 mimics transfection and led to the significant suppression of the cell growth and the induction of apoptosis in LoVo cells in vitro, and the inhibition of tumour growth in vivo. Moreover, the potential targets of miR-26b was predicted by using bioinformatics, and then the predicted target genes were further validated by comparing gene expression profiles between LoVo and NCM460 cell lines. Four genes (TAF12, PTP4A1, CHFR and ALS2CR2) with intersection were found to be the targets of miR-26b. MetaCore network analysis further showed that the regulatory pathways of miR-26b were significantly associated with the invasiveness and metastasis of CRC cells. These data suggest that miR-26b might serve as a novel prognostic factor and a potential therapeutic target for CRC. © 2011 The Authors Journal compilation © 2011 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.

Authors Ma YL, Zhang P, Wang F, Moyer MP, Yang JJ, Liu ZH, Peng JY, Chen HQ, Zhou YK, Liu WJ, Qin HL
Journal Journal of cellular and molecular medicine
Publication Date 2011 Sep;15(9):1941-54
PubMed 20831567
PubMed Central PMC3918049
DOI 10.1111/j.1582-4934.2010.01170.x

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