Tumor Suppressor Functions of miR-133a in Colorectal Cancer
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AbstractDysregulated microRNA (miRNA) expression was profiled through a miRNA array comparison between human colorectal cancer tumors and their adjacent normal tissues. Specifically, using laser capture microdissection, miR-133a was shown to be significantly downregulated in primary colorectal cancer specimens compared with matched adjacent normal tissue. Ectopic expression of miR-133a significantly suppressed colorectal cancer cell growth in vitro and in vivo. Cell-cycle analysis revealed that miR-133a induced a G(0)/G(1)-phase arrest, concomitant with the upregulation of the key G(1)-phase regulator p21(Cip1). We further revealed that miR-133a markedly increased p53 protein and induced p21(Cip1) transcription. Studies in silico revealed that the 3'UTR of the ring finger and FYVE-like domain containing E3-ubiquitin protein ligase (RFFL), which regulates p53 protein, contains an evolutionarily conserved miR-133a binding site. miR-133a repressed RFFL-3'UTR reporter activity and reduced RFFL protein levels, indicating that miR-133a directly bound to RFFL mRNA and inhibited RFFL translation. Moreover, miR-133a sensitized colon cancer cells to doxorubicin and oxaliplatin by enhancing apoptosis and inhibiting cell proliferation. These data add weight to the significance of miR-133a in the development of CRC. (C) 2013 AACR.
All Author(s) ListDong YJ, Zhao JH, Wu CW, Zhang LJ, Liu XD, Kang W, Leung WW, Zhang N, Chan FKL, Sung JJY, Ng SSM, Yu J
Journal nameMolecular Cancer Research
Volume Number11
Issue Number9
PublisherAmerican Association for Cancer Research
Pages1051 - 1060
LanguagesEnglish-United Kingdom
Web of Science Subject CategoriesCell Biology; CELL BIOLOGY; Oncology; ONCOLOGY

Last updated on 2021-18-09 at 23:51