Chemo-Surveillance as a Natural Mechanism to Ensure Perfection of Wound Healing to Avoid Cancer Evolution and to Cure Cancer

The objectives of this study are to explore the interrelationship between wound healing and cancer. This opinion article highlights the mechanism of wound healing and the impact of wound on cancer evolution and cancer therapy. Wound healing requires the proliferation and the terminal differentiation (TD) of progenitor stem cells (PSCs). PSCs are pluripotent stem cells that can be differentiated into a variety of cells to help with wound healing. Compounds implicated in chemo-surveillance and cachexia have a significant impact on wound healing. Wound triggers the production of prostaglandins (PGs) which play an essential role to promote the proliferation of PSCs at the initial stage of the wound. At the final stage of wound healing, chemo-surveillance comes into play to induce TD of PSCs. The functionality of chemo-surveillance dictates the success of wound healing. The functionality of chemo-surveillance is usually intact in healthy people, so wounds typically heal nicely without having to put up any efforts. Wound also triggers production of tumor necrosis factor (TNF) which is responsible for the display of cachexia symptoms leading to the collapse of chemo-surveillance. TD of PSCs will be impaired, allowing PSCs to evolve into cancer stem cells (CSCs). It takes only a single hit to silence TET-1 enzyme to convert PSCs to become CSCs, which is well within the reach of PSCs because MEs of PSCs are abnormally active like cancer cells (CCs) due to association with telomerase. Wound healing and evolution of cancer are so closely related to involve PSCs as the critical common elements. Cancer can arise if a wound is not healed properly. Following a successful wound healing process is the best method for cancer treatment. Cachexia symptoms must be eliminated, chemo-surveillance must be restored, CSCs must be eradicated, differentiation blockade must be eliminated, and oncogenes and cancer suppressor genes must be removed. Wound-healing metabolites are the best candidates to meet these needs.