While driven by genetic mutations, cancer cells are also forced to reprogram their uptake, production and use of nutrients and metabolites to fuel their constant proliferation. This induces in them dependencies that may be exploited for cancer therapy. In a September paper in Cell Metabolism, researchers led by Ludwig San Diego’s Paul Mischel described how an enzyme involved in building cell membranes, LPCAT1, links hallmark changes in the cancer cell’s membrane structure to its metabolic and growth-promoting genetic alterations. Paul and his colleagues discovered that LPCAT1 subtly tweaks the chemical composition of the external cell membrane in a way that boosts the transmission of proliferative signals in cancer cells driven by dysregulated growth factor signaling. Cancers of this sort are notably dependent on the enzyme. When LPCAT1 was genetically depleted in mouse models of multiple types of cancer, including the aggressive brain cancer glioblastoma and lung cancer, tumors shrank dramatically and survival times improved.
This article appeared in the November 2019 issue of Ludwig Link. Click here to download a PDF (1 MB).