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Many cancer cells depend on glutamine as a fuel for proliferation, yet the mechanisms by which glutamine supports cancer metabolism are not fully understood. Two recent studies highlight an important role for glutamine in the synthesis of lipids and provide novel insights into how glutamine metabolism could be targeted for cancer therapy.
Pyruvate kinase catalyzes the transfer of a high-energy phosphate group from phosphoenol pyruvate (PEP) to generate pyruvate and ATP, a reaction that is the rate-limiting step of the glycolytic pathway. The PKM1 alternatively-spliced isoform is ubiquitously expressed whereas the PKM2 isoform is normally highly expressed only in embryos and undifferentiated tissues, correlating with high rates of cellular proliferation. Notably, tumors express the PKM2 form to the exclusion of the M1 isoform.
The zinc-finger DNA-binding protein CTCF has been known for being a constituent of insulators. A recent paper in Nature reports an unforeseen intragenic role for CTCF that links DNA methylation with alternative splicing. By binding to its target DNA site placed within an alternative exon, CTCF creates a roadblock to transcriptional elongation that favors inclusion of the exon into mature mRNA. DNA methylation prevents CTCF binding, which releases pol II transient blockage and promotes exon exclusion.
In patients with malaria, Plasmodium falciparum parasites multiply to enormous numbers in the bloodstream, initiating processes of erythrocyte destruction, endothelial activation and microvascular inflammation that cause devastating pathological effects on host tissues and organs. Recent research casts new light on a mechanism by which hemoglobin mutations may protect against these effects, and on a critical receptor-ligand interaction that provides fresh opportunities for the development of vaccines against blood-stage infection.
