The E2F family of transcription factors plays a critical role in the control of cell proliferation by regulating the timely expression of many genes required for cell cycle progression. E2F activity is essential for cell proliferation and its inhibition leads to cessation of cell growth. In normal cells, E2F is tightly regulated to prevent uncontrolled growth. In cancer cells, its regulation is often abrogated and most human tumors exhibit deregulated and hyperactive E2F leading to uncontrolled cell proliferation.

Transcriptional activation of cell-cycle-related genes is only one facet of E2F activity and one member of this family, E2F1, can also mediate apoptosis. Furthermore a recent study from our lab shows that E2F1 can also induce autophagy. In addition, our studies show that E2F1 can activate a number of major signal transduction pathways including the PI3K/AKT; MEK/ERK, and p38 MAPK pathways.

Work in our lab focuses on elucidation of the molecular mechanism that mediates the effects of E2F on cell fate and intracellular signaling.

Current research topics in our lab are:

1. Studying the mechanisms by which E2F1 sensitizes cells to chemotherapeutic treatments.
2. Studying the crosstalk between E2Fs and signal transduction pathways.
3. Isolation and characterization of novel E2F-regulated genes that affect autophagy. Elucidating the role of E2Fs in the regulation of autophagy.
4. Identification of novel molecular links between E2F1 and the tumor suppressor p53.