SKIN CANCER treatment may soon involve targeting a particular protein, after scientists discovered it could both drive and inhibit tumour growth.
Researchers have identified a particular protein that regulates an enzyme which can both encourage and kill cancerous tumours.
A study by Penn State found that the enzyme – IRE1 – is regulated by a protein called Ras.
In a series of molecular interactions, IRE1 and Ras can drive or inhibit particular cancers.
Scientists discovered this included non-melanoma skin cancer.
The researchers believe the findings could lead to future treatment to help fight cancer. They have gone back to basics to find out how cancer starts and what drives it’s spread.
The researchers believe the findings could lead to future treatment to help fight cancer.
They have gone back to basics to find out how cancer starts and what drives it’s spread.
“What this is really about is learning the basic biology of cancer to discover new ways to target the disease,” said Adam Glick, a professor of veterinary and biomedical sciences at Penn State.
“The more we know about the molecular circuitry — and the mutations and genetics of cancer — the more we can design drugs that specifically target cancer cells without harming normal cells.”
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Researchers are still in the process of working out how the protein does this.
“We still don’t know how Ras is causing the stress response, whether because the cells are more proliferative, or because of other unknown factors outside or inside the cell, but the end result seems to be increased unfolded proteins in the endoplasmic reticulum (ER),” said Glick.
A build-up of incorrectly folded proteins in the ER – a region of the cell – activates IRE1, which then tries to reduce this unfolded stress response.
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“While this action of IRE1 helps cells survive and may promote cancer development, one of the targets for this messenger RNA degradation pathway actually encodes an oncogenic protein, called Id1,” said Glick.
“It turns out that IRE1 has both pro-oncogenic and tumour-inhibiting capabilities that, by degrading this message, can counteract the tumour-promoting effects of oncogenic Ras.
“The end result is cells don’t continue to proliferate and undergo a process called senescence, or accelerated ageing. Basically, they die.”
It is the first time a link has been made between Ras and the double role of IRE1 in cancer.
“What this says to us is that possibly, by manipulating IRE1 we can potentially drive tumour cells to self-terminate,” said Glick.