Epigenetic Changes Due to Aging May Lead to Cancer

Throughout our lives, all cells in our bodies experience a normal life cycle of growth, maturity, and death. During this time, our cells normally experience damage to DNA by normal functions of the metabolism, or exposure to certain environmental factors like UV light. Ordinarily, our body is able to repair the damage done to the DNA in order to restore healthy cell function. The older we get, the more DNA damage we experience, and if damaged DNA is unable to be repaired, the cells become more susceptible to continued, erratic cell division, which often results in cancer. The cells of the body undergo a general wearing out process known as cell senescence, in which the cell ceases to replicate and is programmed for death. Senescence is a healthy, highly regulated process, and is crucial in the protection against tumour-growth.

It was previously considered by scientists that cancer development arises from rogue damaged cells that escape the natural cell death process and continue on to divide and grow. But scientists discovered that epigenetics could play a large role in how normal cells can develop into tumour-promoting cells.

“Senescence is a very well-known, normal aging process that is actually an antitumor mechanism. It occurs when cells perceive an excess of DNA damage, when cells undergo too many cell divisions or when they experience cancer development-related stress. They focused their attention on DNA methylation patterns in the fibroblasts of human foreskin samples how it can disrupt normal cellular senescence, allowing the progression of tumour growth. DNA methylation is the epigenetic process that silences gene expression by adding methyl groups to the DNA sequence, making it an appropriate target for studying the healthy function of the cellular death process.

The researchers also allowed a second group of healthy fibroblast cells to mature into natural cellular senescence, and observed the DNA methylation patterns in both groups