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Under the microscope: The G protein-coupled estrogen receptor

Tell me about this receptor
The G protein-coupled estrogen receptor (let’s call it the GPER) is a seven-transmembrane-domain receptor that mediates non-genomic estrogen-related signalling.

How does it work?
After ligand activation, GPER triggers multiple downstream pathways that exert diverse biological effects on the regulation of cell growth, migration and programmed cell death in a variety of tissues. 

Does that means it has some kind of relationship with cancer progression?
Bingo. As such, a better understanding of the role GPER plays in cancer biology may lead to the identification of novel therapeutic targets.

So this has been in the news then?
Yes, new US research shows that activating the GPER can not only stop pancreatic cancer from growing, but may also make tumours more visible to the immune system and thus more susceptible to modern immunotherapy.

How does the use of GPER activators differ from other anti-cancer agents?
Nearly all current cancer drugs act to block the activity of cellular proteins that are needed by not only the cancer cells, but also by normal cells. As a result, most cancer drugs are associated with major toxicity.

How does this differ?
Using the estrogenic analogue to activate GPER mirrors something that naturally occurs in the body, as GPER is already present and normally activated by estrogen, especially in women during pregnancy.

What are the implications of its natural occurrence?
As it is something the human body is already accustomed to, evidence from preclinical animal studies suggested that side effects to this approach would likely be minimal, if this procedure moves into clinical practice.

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