Fig. 3

Some of the underlying molecular mechanisms for colorectal cancer bacteriotherapy. The whole cell bacteria (especially Lactic acid bacteria known as LABs) may lead cancer cells to apoptosis through intrinsic or extrinsic pathways. Bacterial peptides such as arenamides can prevent TNF-induced expression of pro-inflammatory mediators by NF-κB pathway blockage. Bacterial toxins such as C. perfringens enterotoxin (CPE) can directly interact with claudin-3 and claudin-4, which are over-expressed in colorectal cancerous cell membrane. This attachment results in pore formation through the membrane and cell death due to loss of cellular osmotic equilibrium. Another mechanism for bacterial toxins’ anti-cancer effect is cytotoxicity through apoptosis intrinsic pathway. Bacteriocins such as nisin are able to form membrane-pores when they bind to special type of cell surface receptors which cause leakage of cellular content and cell death. Besides pore formation activity, bacteriocins may act as apoptosis initiator through the intrinsic pathway [10, 16, 30, 50, 65, 68, 69]