Scientists at the Medical Research Council (MRC) Cancer Cell Unit, at the University of Cambridge, have revealed a new insight into how our body cells block the development of cancer.
The finding, published in this month’s edition of Nature - Structural and Molecular Biology, sheds light on how some widely used cancer treatments work through natural processes in the body. This may help scientists develop new and improved cancer therapies in the future.
The research team discovered that two proteins, known to be involved in tumour suppression but previously thought to function independently, work together to prevent cells from becoming cancerous. They act by ‘supervising’ the process of cell division so that it starts and stops at the right time and in the right amount for normal growth and development to take place. If the proteins fail to work together, the cell will continue to divide and multiply abnormally and may form a cancerous tumour.
Commonly used cancer treatments such as Taxol work through these proteins to control cell division and prevent the multiplication of cancer cells. Unravelling how the proteins function together may help researchers understand more about how cancer treatments work and why some cancer cells are resistant to them.
The team found that if a protein called CHFR moves through structures made by another protein called PML during cell division, equal amounts of DNA are distributed to each of the two daughter cells. If this doesn’t happen, the genetic information is shared unequally and the daughter cells may not inherit the complete set of the ‘checks and balances’ they need to tell them when to ‘switch off’ the process of cell division.
The research team was led by Professor Ashok Venkitaraman, Deputy Director of the MRC Cancer Cell Unit and member of the University of Cambridge Cancer Research UK Department of Oncology.
Professor Venkitaraman said:
“How cancers respond to widely used medicines is not well understood. To find that these responses depend on two proteins that are frequently abnormal in cancer cells is exciting, and could in the future lead to improvements in cancer therapy.”
Matthew Daniels, at the University of Cambridge, worked on the project with Professor Venkitaraman. He said:
“We are starting to build models of cancer based on where key processes at the molecular level go wrong. This kind of understanding is essential if we are to target the disease effectively in the future.
The research was funded by the MRC and an AstraZeneca studentship to Cambridge University Clinical School.