KLF8, or Kruppel-like factor 8, is known to be involved in cancer. Scientists at the University of Central Florida have recently discovered a role for this protein in DNA repair, a process that allows cells to correct damaged parts of their DNA.
DNA damage occurs naturally, and can also be a result of carcinogens or environmental stresses. The cell copes with minor DNA damage by activating repair processes that replace the damaged sections. If a cell’s DNA becomes damaged beyond repair the cell enters a suicidal “cell death program“. This is a protective measure preventing the formation of cancerous cells harbouring harmful mutations as the damaged DNA will perish with the cell. The space left by the death of the cell will be filled by healthy neighbouring cells and so organs and tissues remain healthy.
Cancer treatments in the past have used drugs that damage the DNA, causing cancer cells to enter the cell death program. However, it is now known that cancer cells often have increased expression of proteins involved in DNA repair, allowing the survival of damaged cells. In this case DNA damaging drugs can actually increase the rate at which cancer cells are transformed, or changed, towards being more aggressive and malignant, as the cells no longer perish under the pressure of DNA damage. New treatments aim to target the cancer cells DNA repair mechanisms so they can no longer continue to survive with damaged DNA.
Research by Lu and colleagues have discovered that the KLF8 protein is overexpressed in breast cancer. This protein, with other DNA repair proteins, is involved in cancer cell survival. Their finding shed light on a new way to target cancer cells by targeting the protective properties of DNA repair.
This research is published in the Journal of Biological Chemistry and can be viewed, as a free article at http://www.ncbi.nlm.nih.gov/pubmed/23105099
Lu, Heng, et al. “A novel role of Kruppel-like factor 8 in DNA repair in breast cancer cells.” Journal of Biological Chemistry (2012).