A growing body of literature evaluated the prognostic value of ALDH1L1 expression for cancer disease, the regulatory role of the enzyme in cellular proliferation, and associated metabolic and signaling cellular responses.
This review discusses the role of ALDH1L1 in folate metabolism and etiology of diseases with the focus on non-synonymous coding <i>ALDH1L1</i> SNPs and their effects on the enzyme structure/function, metabolic role and association with cancer.
This review discusses the link between folate and cancer, modifying effects of alcohol consumption on folate-associated carcinogenesis, and putative roles of ALDH1L1 and ALDH1L2 in this process.
Our second hypothesis is that folate interacts with one of these response elements to upregulate ALDH1A1 and ALDH1L1 expression in order to decrease acetaldehyde concentrations and promote DNA stability, thereby decreasing cancer susceptibility.
10-Formyltetrahydrofolate dehydrogenase (FDH) suppresses cancer cell proliferation through p53-dependent apoptosis but also induces strong cytotoxicity in p53-deficient prostate cells.
We have recently shown that transient expression of 10-formyltetrahydrofolate dehydrogenase (FDH) strongly inhibits proliferation of several cancer cell lines and ultimately results in cell death.