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Regulation of G1 Cell Cycle Progression in Cancer - Cell cycle progression from early G1 to late G1 and then into S phase requires both increased cellular growth, resulting in an accumulation of mass, and the concerted activities of multiple cyclin-dependent kinases (cdk), cdk inhibitors and tumor suppressors. The vast majority of malignant cells selectively target these pathways for alteration. Our lab is focused on determining the consequences of these genetic and epigenetic alterations and the mechanism that cell growth activates the cell cycle machinery.

We are also interested in the delivery of novel anticancer macromolecular therapeutics. Delivery across the cell membrane is generally restricted to small molecules less than 500 Daltons in size. However, peptides, proteins, siRNAs are in vast excess to this bioavailability limitation. Consequently, we have focused a lot of our attention on delivery by cationic protein transduction domains (PTDs)/cell penetrating peptides (CPPs), such as the TAT peptide. Our recent work has uncovered the mechanism that these peptides enter cells, namely macropinocytosis, a specialized form of fluid phase endocytosis, and devised methods to enhance endosomal escape. In addition, we have generated peptides that target cell cycle regulatory proteins to treat mouse models of metastatic ovarian cancer.

Track(s):
MCB
Molecular Pathology

BMS Focus Areas:
Cancer Biology