Prostate cancer progression is now known to depend on the non-tumour ‘bystander cells’ surrounding the tumour cells. The mechanism(s) whereby non-tumour-bystander-cells affect tumour cells is not yet understood. We propose that this effect of bystander cells on tumour cells,or of tumour cells on the bystander-cells, is mediated by 1. Substances secreted by the bystander-cells and/or tumour cells that cross-over and regulate their neighbouring cells or 2. The bystander-cell-secreted material on which the tumour cells grow. This bystander-cell-secreted material on which tumour cells ‘sit/grow’ affects tumorigenesis. Neither the nature of the bystander-cell-secreted factors affecting prostate cancer cells nor the stimuli that promote secretion of compounds from the bystander-cells are yet known. We hypothesise that these bystander-cell/tumour-cell-secreted compounds cause cell-to-cell communication conveyed by digestive enzymes that activate cell signals by cutting/turning-on a specialized ‘cell-surface-receptor-on-switch’ (a digestive-enzyme-activated-receptor) on both the tumour cells and non-tumour bystander cells. We will evaluate these possibilities using human prostate-tissue-derived bystander-cells, determining 1.If they secrete enzymes that regulate the ‘on-switch’ on prostate-cancer-derived cells and 2.If the ‘on-switch’ in prostate-derived bystander-fibroblasts responds to tumour-cell-secreted digestive enzymes by producing secreted material on which the tumour cells grow more aggressively. The data may reveal new ways to control prostate tumour development.