American Association for Cancer Research
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Supplementary Table 1 from Tumor Suppressor Functions of miR-133a in Colorectal Cancer

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posted on 2023-04-03, 16:04 authored by Yujuan Dong, Junhong Zhao, Chung-Wah Wu, Lijing Zhang, Xiaodong Liu, Wei Kang, Wing-Wah Leung, Ning Zhang, Francis K.L. Chan, Joseph J.Y. Sung, Simon S.M. Ng, Jun Yu

PDF file - 48K, Characteristics of the CRC patients for miRNA array.



Dysregulated microRNA (miRNA) expression was profiled through a miRNA array comparison between human colorectal cancer tumors and their adjacent normal tissues. Specifically, using laser capture micro-dissection, 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 G0/G1-phase arrest, concomitant with the upregulation of the key G1-phase regulator p21Cip1. We further revealed that miR-133a markedly increased p53 protein and induced p21Cip1 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.Implications: miR-133a serves as a potential tumor suppressor upstream of p53 in colorectal cancer and may sensitize cells to therapeutics. Mol Cancer Res; 11(9); 1051–60. ©2013 AACR.

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