AI Article Synopsis
- The RNA-binding protein HuR's expression and levels increase in colon cancer tissues compared to normal tissues.
- Modulating HuR levels in colon cancer cells impacts gene expression and identifies beta-catenin mRNA as a new target of HuR.
- Overexpression of HuR in cells leads to larger tumor growth in mice, while reducing HuR slows down tumor development, indicating its key role in colon cancer progression.
Article Abstract
Immunohistochemical analysis of paired tumor and normal tissue specimens revealed that the expression and cytoplasmic abundance of the RNA-binding protein HuR increased with malignancy, particularly in colon carcinomas. Interventions to modulate HuR expression in human RKO colon cancer cells altered gene expression profiles and identified beta-catenin mRNA as a novel HuR target. Subcutaneous injection of HuR-overexpressing RKO cells into nude mice produced significantly larger tumors than those arising from control populations; conversely, RKO cells expressing reduced HuR through small interference RNA- or antisense HuR-based approaches developed significantly more slowly. We propose that HuR-regulated target mRNA expression contributes to colon cancer growth. Our results suggest a pivotal function for HuR in colon carcinogenesis.
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| http://dx.doi.org/10.1038/sj.onc.1206862 | DOI Listing |
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