The Daily Bulletin

Please join the Biology Department and the Great Lakes Center for the seminar "Disruption of the Molecular Circadian Clock in Cancer," presented by Brian J. Altman, assistant professor in the Department of Biomedical Genetics at the University of Rochester Medical Center, on Monday, September 23, from 3:00 to 3:50 p.m. in Technology Building 160. All students, staff, and faculty are welcome.

Abstract
Circadian rhythms are 24-hour cycles present in most eukaryotes that govern many physiologic and molecular processes, including global gene expression and metabolism. These cycles serve to balance energy expenditure to the day/night cycle and are governed by a complex transcriptional/translational feedback loop known as the "molecular clock." While the molecular clock connects somatic cells to external timing stimuli, its role in cancer is still not well understood. Epidemiological studies have long suggested that circadian disruption in night-shift workers results in a higher incidence of cancer, and recent analyses suggest that oscillation of the clock is lost in human lung cancer. Previously, we demonstrated that the MYC oncoprotein disrupts the molecular clock by inducing the negative regulatory factors REV-ERBα and REV-ERBβ in cell models representing a bone cancer, liver cancer, and nerve cancer. Lung cancer is responsible for the most cancer deaths annually in the United States, and the circadian clock is known to be a tumor suppressive process in lung cancer. Building off the observation that MYC-family mutations occur early in the development of lung cancer and correlate with poor prognosis, we set out the study to the role of MYC in control of the circadian clock in lung cancer. Our recent findings suggest that oncogenic MYC disrupts the clock in the normal lung, and lung cancer cells become dependent on clock dysfunction for growth. In the future, these studies will lay the groundwork for potentially utilizing existing molecular clock targeting agents to restore clock function and slow growth of lung cancer.