Question

Ether lipid levels are higher in tumors, but their specific function in cancer has remained unclear. We show here that the metabolic enzyme alkylglyceronephosphate synthase (AGPS), a critical step in the synthesis of ether lipids, is up-regulated across multiple types of aggressive human cancer cells and primary tumors. Inactivation of AGPS leads to significant impairments in cancer pathogenicity through not only lowering the levels of cellular ether lipids, but also by altering fatty acid, eicosanoid, and glycerophospholipid metabolism, resulting in an overall reduction in the levels of several oncogenic signaling lipids.

What does this mean?

Why is it significant?