Across a wide variety of cancer types, a protein called KRAS can get hyperactivated and transmit an overload of unwanted growth signals to the cells, causing them to divide and form a tumor.
A tumor doesn't just contain cancer cells, though. It also has some non-cancer cells in there, such as immune cells and fibroblasts (cells that make the dense support structure that keeps cells stuck together).
Research by Chris Tape, Claus Jørgensen and colleagues at The Institute of Cancer Research, London, MIT, the Cancer Research UK Manchester Institute and The University of Manchester, has shed some new light on how mutated KRAS causes cancer cells to grow by promoting three distinct ways of cellular signaling:
- Through a direct signaling pathway within the cancer cell, with KRAS signaling through the classic RAS-RAF-MEK-ERK signal transduction cascade, this is called cell-autonomous signaling.
- By inducing the cancer cell to release a protein called SHH, which is able to start specific signaling pathways inside the fibroblast cells. This is called non-cell-autonomous signalling.
- When these non-cell-autonomous signaling pathways in the fibroblast cells are induced, the fibroblasts are able to release growth factors that go back to the cancer cell, where they initiate more growth signaling pathways through a PI3K-AKT signal transduction cascade.
Uncovering these new ways in which mutated KRAS is able to promote cancer cell growth by hijacking fibroblast cell signaling could lead to new possibilities for therapeutic intervention.
This video was originally published by Phospho Biomedical Animation on 14/04/16 here.
This content has been adapted from materials provided by The ICR London. Note: material may have been edited for length and content. For further information, please contact the cited source.