UAlberta Math Biology Seminar: Katrin Schroeder

Reactive oxygen species (ROS) often get a bad reputation. They are linked to cancer formation and contribute to aging—not just of the skin but throughout the body. Given these harmful effects, it might come as a surprise that living organisms actively produce ROS through a specialized group of enzymes: the NADPH oxidases (Nox family). These enzymes serve crucial roles in both normal physiology and disease. In the short term, ROS act as signaling molecules, enhancing cellular communication and amplifying immune responses. Over longer timescales, they contribute to essential processes like maintaining cell balance and guiding cell differentiation.

One key player in this system is NoxO1, a component of the Nox1 complex. Unlike other ROS-producing enzymes, NoxO1 drives continuous ROS formation. This activity is particularly important in the colon, where NoxO1 regulates the differentiation of enterocytes—the cells lining the intestinal wall. Mice lacking NoxO1 are more prone to developing colon cancer, highlighting its protective role. Beyond ROS production, NoxO1 interacts with Erbin, a protein linked to ErbB2 (also known as HER2)—a well-known marker of aggressive breast cancer. Intriguingly, NoxO1 overexpression reduces the abundance of the EGF receptor (EGFR) and enhances its interaction with Erbin. As a result, cancer cell proliferation driven by EGF (epidermal growth factor) is suppressed. Additionally, NoxO1 influences the formation and processing of endosomes and lysosomes, cellular structures essential for EGFR turnover and EGF uptake. Though the exact mechanisms remain unclear, these findings suggest that NoxO1 may represent a novel target for cancer therapy.

This talk will explore the (patho-)physiological roles of NoxO1 and discuss exciting future directions in this evolving field.