Gina L. Razidlo, PhD

Overview

Aim: Basic Science / Cancer Biology

Pancreatic cancers have high demands for energy to fuel tumor growth and metastasis, the spread of cancer throughout the body. The processes of tumor cell migration and invasion are highly energy intensive, and often occur in nutrient-poor environments. To overcome this, cancer cells have altered metabolism and are able to switch their usage of energy sources to drive tumor progression and metastasis. Tumor cells have increased access to excess fats through multiple mechanisms, for example, through increased lipid synthesis or through increased availability of extracellular fatty acids due to obesity. Indeed, obesity is a risk factor for pancreatic cancer, in addition to other tumor types. Intracellular fatty acids are stored in specialized organelles called lipid droplets (LDs). We have found that tumor cells can utilize these increased lipid stores to fuel tumor cell invasion and metastasis. By interfering with the utilization of these lipids, we predict that we could selectively cut off a tumor’s fuel source and reduce metastasis and tumor progression. We hope to determine how these stored lipids contribute to pancreatic cancer progression and metastasis, with the goal of identifying new targets for inhibiting the energy usage by cancer cells.