Grant: Master's Award: Canada Graduate Scholarships

Cells that are in contact, as in tissues, may communicate via small transmembrane pores termed gap junctions. This intercellular communication is critical for regulation of normal cell processes such as growth, proliferation, and programmed self-destruction; in transformed (cancerous) cells, this type of intercellular communication is often blocked. Infection of normal liver cells with different mutated forms of a specific viral oncoprotein (the middle T antigen of polyoma virus) produced transformed cell lines that differed in their activation of specific intracellular signalling cascades, and, therefore, the dominant intracellular signals. The effects of these different signals on gap junctional permeability -- that is, whether the signals allow or prohibit gap junctional intercellular communication -- will be studied in said cell lines using a novel electroporation technique. Identifying both the signalling cascades and the specific signalling proteins that are responsible for the inhibition or promotion of gap junctional intercellular communication may provide us with potential therapeutic targets in the development of new cancer chemotherapies, as drugs that either block the aforementioned inhibitory signals, or stabilize the promotional signals, may be able to reinstate effective gap junctional intercellular communication. This kind of treatment could, in theory, slow the growth of, and promote the self-destruction of, tumour cells alone, rendering the healthy tissues of cancer patients unharmed.