Laforin confers cancer resistance to energy deprivation-induced apoptosis.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 18519661.
- Also identified by DOI 10.1158/0008-5472.CAN-07-6314 and PMC identifier 2440919.
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Abstract
A long-standing but poorly understood observation in experimental cancer therapy is the heterogeneity in cancer susceptibility to energy deprivation. Here, we show that the hexose kinase inhibitor 2-deoxyglucose (2-dG) preferentially kills cancer cells with defective laforin expression and significantly increases the survival of mice with aggressive lymphoma due to a genetic defect of the laforin-encoding Epm2a gene. Normal cells from Epm2a(-/-) mice also had greatly increased susceptibility to 2-dG. Thus, laforin is a novel regulator for cellular response to energy deprivation and its defects in cancer cells may be targeted for cancer therapy.
Medical subject headings
- Apoptosis
- Energy Metabolism
- Protein Tyrosine Phosphatases, Non-Receptor