HMGB1, a crucial player that links wound healing and cancer risk

Already in the nineteenth century, it has been proposed that chronic inflammation or previous injury can predispose tissues to tumor formation. It is still not fully understood however, what cell types and mechanisms explain this link. 

In this context, VIB-UGent/CRIG researcher Dr. Esther Hoste (of the lab of Prof. Geert van Loo) and colleagues studied HMGB1, a molecule that is secreted by damaged tissue and activates the immune system. The scientists found that genetic deletion of HMGB1 in epithelial skin cells of mice fastened wound healing and completely protected mice from wound-induced tumor formation. Moreover, skin wounds of those mice showed less neutrophils, short-lived immune cells that are the first to enter the skin after injury and can form specialized structures termed NETs (neutrophil extracellular traps).

‘We demonstrated that a mechanism used to alarm your immune system that something is going wrong, can be hijacked for cancer initiation', says Dr. Hoste. ‘While secretion of HMGB1 is a good thing in conditions of minor injury, it can be a harmful event in more serious or chronic wounds as it can trigger tumor formation at these wound sites. This really is a case of too much of a good thing can hurt you.’

The study suggests that HMGB1-focused therapies could accelerate wound healing responses (f.e. in blistering diseases or in diabetic patients with chronic ulcers), while limiting the risk of cancer initiation.

Read more via this link.

The study was recently published in the journal ‘Cell Reports’ and is accessible via this link.