Primary Research Focus
The basis for much of the work in the Miskimins Lab is the “reprogramming” of cancer cell metabolism. For energy metabolism most normal tissues and cells use carbohydrates, proteins and fats which are processed to maximize ATP production. In contrast, cancers rely heavily on carbohydrate, primarily glucose and metabolism. Cancer cells use glucose to produce energy, but they also use the carbon chains of glucose to produce the “building blocks” needed to make new cells. They also rely on metabolism of certain amino acids for growth. The lab’s current research focuses on understanding the regulation of these metabolic pathways and how they can be manipulated to alter the properties of tumors.
A main research interest in the Miskimins lab is tumor cell metabolism. Cancer cells undergo a process called metabolic reprogramming that allows them to survive and proliferate under conditions that would be detrimental to normal cells. By modulating the altered metabolic processes, it may be possible to specifically target cancer cells and inhibit their growth and promote their death. The team has found that several drugs or compounds that alter specific metabolic pathways are toxic to cancer cells. One of these drugs is metformin, which is commonly used for treating type II diabetes. In cancer cells, metformin inhibits cell proliferation and then promotes cell death. The lab is analyzing the mechanisms that lead to these cellular responses. The goal is to determine the molecular pathways that mediate these effects. The Miskimins lab is also identifying other metabolism-targeted drugs and compounds that synergize with metformin to kill cancer cells.
About the Miskimins Lab
Lab Projects and News
BMC Cancer
Project Title: Knockdown delta-5-desaturase in breast cancer cells that overexpress COX-2 results in inhibition of growth, migration and invasion via a dihomo-γ-linolenic acid peroxidation dependent mechanism.
Role: Project Co-Principal Investigator
This is an investigation to understand if a high level of COX-2 in breast cancer cells can be capitalized on inhibiting cancer growth and migration. The outcome of this translational research could guide us to develop new anti-cancer strategy and/or to improve current chemotherapy for breast cancer treatment.