The organs and tissues in our bodies are formed by a vast number of cells, which altogether co-ordinate their actions for our body to function properly. However, a number of 'abnormal' cells have previously been found in tissues derived from old patients and at the initial stages of cancer.
These particular cells suffer a growth arrest termed 'senescence', which is thought to affect how the tissue functions. Senescent cells fail to proliferate, but they manage to communicate with their neighboring cells, mainly through the release of inflammatory proteins.
The study, published inCell Reports, describes a new way that senescent cells communicate, which is via the expression of integrin membrane proteins, including a protein called 'integrin beta 3' which is highly expressed during senescence.
b3 expression accelerates the onset of senescence in human primary fibroblasts by activating the transforming growth factor b (TGF-b) pathway in a cell-autonomous and non-cell-autonomous manner. b3 levels are dynamically increased during oncogene-induced senescence (OIS) through CBX7 Polycomb regulation, and downregulation of b3 levels overrides OIS and therapy-induced senescence (TIS), independently of its ligand-binding activity.
They could also see that integrin beta 3 was 'upregulated' in a subset of tissue from mice, confirming the importance of their results in two different species.
Lead researcher said: "This is the first time that integrin beta 3 has been identified in the context of senescence and ageing, and could be in the future a potential therapeutic target during early carcinogenesis and ageing.
"This finding is particularly interesting, as there is actually a drug against integrin beta 3, called 'cilengitide', that averts one of the disadvantages of ageing in our model - inflammation. It does this without increasing cell proliferation, which is an advantage, as an increase in cell proliferation imposes a risk for cancer."