KLF4 has been implicated in many different types of cancer. However, its ability to act as a tumor suppressor or oncogene is tissue and context specific. In Mouse Embryonic Fibroblast cells (MEFs) and Colorectal Cancer, klf4 has been shown to act as a tumor suppressor. Previously, our lab has shown that cells lacking Klf4 exhibit increased rates of glycolysis, as well as impaired mitochondrial bioenergetics including increased proton leak and decreased maximal respiratory capacity. However, the mechanism by which KLF4 regulates glycolytic metabolism is not well understood. Using different molecualr and cellular teachniques, we will examine whether cells lacking Klf4 exhibit increased expression of the glucose transporter proteins GLUT1 and SGLT1, as well as the glycolytic regulatory enzymes such as Hexokinase II (HK2).
The aims of this project are as follow:-
To determine metabolic status of Klf4-expressing and –deficient colorectal cancer cell lines.
To test whether loss of Klf4 supports a switch from oxidative phosphorylation to glycolysis, and thus is a significant contributor to the Warburg effect
Knowledge of cell culture
Must completed Biol182
Number of Student Researchers
Applications open on 01/03/2021 and close on 03/22/2021