cell loss during injury and cellular damage the failure to eradicate large tumors by cancer drugs is at least partly explained by the acsc signaling this disclosure demonstrates that as cancer cells succumb to apoptosis they are promoting proliferation in their surrounding cells thus reducing the efficacy of treatment moreover an acsc producing cell could potentially disrupt normal tissues by inducing non dividing normal cells in a tissue to lose contact with other cells while undergoing mitosis this would create an opportunity for cancer cells to invade tissues thus enhancing metastasis the donor and the recipient cells will be separated in order to directly examine the molecular events that occur in each cell type during acsc signaling pa requires and thrives in wounds and has evolved virulence mechanisms to inhibit wound healing in particular exotoxin t exot plays a pivotal role in the inhibition of wound healing by pa exot is a bifunctional toxin possessing a gtpase activating protein gap domain at its n terminus and an adp ribosyltransferase adprt domain at its c terminus exot contributes to the inhibition of wound healing by two novel and distinct virulence functions i it blocks host cell division by targeting cytokinesis at multiple steps and ii it prevents pro inflammatory necrotic cytotoxicity while re routing its target host toward silent apoptotic demise data not shown the mechanisms by which exot exerts these two activities remain largely undetermined is demonstrated that exot is both necessary and sufficient to induce apoptosis in target.