What is it about?
If we just turn-off the growth signals at the plasma membrane, cancer cells would stop growing, but if you stop the inhibitor treatment, they will start to grow. That necessitates continued the inhibitor treatment often with a nasty side effects for a long time. But these growth signal receptors actually activate two signaling pathways: the pro-growth signal (Ras-ERK pathway) is to activate cell division pathways such as DNA synthesis and cell cycle machineries, while the pro-survival signal (PI3K-AKT pathway) activates lipids and macromolecule synthesis necessary for cell division. By disrupting cholesterol at the plasma membrane, we can only inhibit pro-survival pathways. Then activated growth signal receptor trigger cell division without necessary components, causing catastrophic cell divine and die.
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Why is it important?
In cancer treatment, it is important that we kill cancer cells, not just arrest their growth. One way to do that is to let the growth signal receptor activated, but disrupt cholesterol at the plasma membrane so that cancer cells would proceed with catastrophic cell division and die.
Perspectives
The signals from activated growth signals bifurcate: from their cytoplasmic tail, it activates Ras-ERK, sending signals straight to the nucleus, while PI3K sitting next to the growth signal receptors at the plasma membrane is also activated, but needs cholesterol at the plasma membrane to recruit AKT to the plasma membrane to generate the pro-survival pathway.
Ryuji Yamaguchi
Kansai Medical University
Read the Original
This page is a summary of: Targeting cholesterol with β-cyclodextrin sensitizes cancer cells for apoptosis, FEBS Letters, November 2015, Wiley,
DOI: 10.1016/j.febslet.2015.11.009.
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