The breast cancer microenvironment and lipoprotein lipase: Another negative notch for a beneficial enzyme?

The energy demand of breast cancers is in part met through the beta-oxidation of exogenous fatty acids. Fatty acids may also be used to aid in cell signaling and toward the construction of new membranes for rapidly proliferating tumor cells. A significant quantity of fatty acids comes from the hydrolysis of lipoprotein triacylglycerols and phospholipids by lipoprotein lipase (LPL). The lipid obtained via LPL in the breast tumor microenvironment may thus promote breast tumor growth and development. In this hypothesis article, we introduce LPL, provide a meta-analysis of RNAseq data showing that LPL is associated with poor prognosis, and explain how LPL might play a role in breast cancer prognosis over time.

Automated summary

The energy demand of breast cancers is partly met by the oxidation of exogenous fatty acids. Fatty acids also play a role in cell signaling and membrane construction for tumor cells. Lipoprotein lipase (LPL) hydrolyzes lipoprotein triacylglycerols and phospholipids to provide fatty acids, which may promote breast tumor growth in the tumor microenvironment.