Abstract

Retinoids and its derivatives are known to regulate tumor progression. Our previous study in Colorectal Cancer (CRC) has shown that the expression of LRAT, a gene converts excess retinol into retinyl ester to balance retinoids homeostasis, may be regulated by its promoter methylation status to modulate the retinoids synthesis. In this report, we begin to explore the potential mechanism of LRAT mediated retinoid metabolism. Our data indicate CRC patient of LRAT hypermethylation associated with better prognosis. A consistent finding is shown in siRNA mediated LRAT silencing, which leads to slow growth of CRC cell lines. We have also observed favorable CRC prognosis occurred in patients of both LRAT and RAR beta hypermethylation, suggesting the better CRC prognosis may be mediated through RAR beta independent pathway.

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