One major difference between cancer cells and normal healthy cells is how they use sugar. Cancer cells show enhanced uptake and use of glucose to both generate energy and to supply all the building blocks needed to rapidly make new cancer cells.
p53, also known as ‘the guardian of the genome’ because it protects against DNA damage, is a tumour suppressor protein that can, amongst other things, restrict this use of glucose and prevent the growth of cancerous cells.
p53 is often mutated in breast cancer and these mutations can stop the p53 protein from working, leading to tumour growth.
In his paper published in Science Signalling, Against Breast Cancer research team member based at the University of Southampton, Dr Charlie Birts describes an important process whereby another protein in the cell, called CtBP, can detect how much glucose a cell is using, and use this information to control the levels of p53.
In tumour development, this process helps select for mutations to occur in the p53 protein. This is highly relevant to breast cancer biology as mutations in p53 permits cells to rely more heavily on glucose, allowing them to rapidly proliferate and survive.
This has further highlighted CtBPs as potential therapeutic targets against breast cancer and particularly those tumors in which p53 no longer works.Read the scientific abstract