Eric Prossnitz, a professor in the Department of Internal Medicine at the Health Sciences Center, has spent his career studying the invisible and complex business of cell signaling.

Taking place in his lab at UNM’s Comprehensive Cancer Center is a foray into the study of how one gene, GPER, plays an important role in the body. A recent discovery by Prossnitz and his team has found that this gene holds some of the secrets of the processes of aging and cancer.

Roughly 10 years ago, the GPER gene was identified as a component in the regulation of estrogen.

While estrogen plays a pivotal part in many bodily systems — including metabolism, insulin regulation and bone growth — it’s also a factor in the development of breast tissue.

“Breast tissue has to be continuously sensitive and ready, if the hormones are there, to expand, which means all these cells have to grow and proliferate,” Prossnitz said.

While this is integral to puberty and the production of milk during pregnancy, the sensitivity that breast tissue employs to its surrounding hormones leaves it more vulnerable than other tissues.

If the hormones, like estrogen, that tell breast tissue to proliferate go unchecked, breast cancer can develop.

“Cancers are diseases where the regulation of cell growth becomes uncontrolled,” he said.

This is where drugs like Tamoxifen come into play, by helping to curb the development of breast tissue cells.

A counteraction of these medicines, though, is the over stimulation of the GPER gene.

“We think this compound helps these cells learn how to survive,” Prossnitz said.

He believes by developing a drug that dampers GPER’s effects on the body, they could halt the breast tissue cells’ survival. With the discovery of the G36 inhibitor, a chemical that does exactly that, they are on their way to developing this drug.

With this potential medication, doctors could employ a double-combatant approach, halting the production of breast cancer cells as well as lowering the cell’s survival rate.

The development of breast cancer isn’t the only realm that GPER plays a part in though; it could also hold the key to slowing the aging process.

This discovery by Prossnitz and his researchers took place in part by chance.

Prossnitz’s team conducted a trial to make side-by-side comparisons of normal mice with Knock-Out mice — mice that had been genetically altered to remove the GPER gene.

They discovered that the mice without the GPER gene had higher rates of obesity and diabetes.

Because of the role estrogen plays in these diseases, and the lack of estrogen caused by removal of the GPER gene, this finding wasn’t unexpected.

What did come as a surprise was that, as the altered mice aged, they showed lower signs of cardiovascular issues.

“We expected their blood vessels and their hearts would be more diseased, show greater signs of aging. They looked great, they were as healthy as a young mouse would be,” Prossnitz said. “This was very odd.”

This discovery led to the realization that the GPER gene wasn’t just an estrogen receptor. It also regulates a protein called NOX1, responsible for creating a substance called superoxide, a reactive oxygen species that causes cellular deterioration.

“Aging is a result of exposure to these reactive oxygen species over a lifetime,” Prossnitz said.

This cellular damage is an integral part of the aging process.

As our cells become damaged and die they are replaced with a material, extracellular matrix, in a process called fibrosis.

Prossnitz described this material as a “scar tissue of the organs.”

“A heart’s job is to pump, but if it’s cells are being replaced with this matrix, it’s not going to do that very well”, he stated.

Because the Knock-Out mice in this trial were lacking the GPER gene, and the cellular damage caused by the production of superoxide, their cardiovascular systems weren’t overloaded with fibrosis.

“It’s a proof of principle that says it could work in humans,” Prossnitz said.

Prossnitz and his team are currently testing the process of GPER and superoxide production in human tissues.

By dampening down the GPER effects using the G36 chemical inhibitor, the team has been able to produce the same results as the trial with mice, limiting the gene expression of NOX1 and thus the amount of superoxide and cellular damage.

In regards to his plans for this discovery, Prossnitz said, ”Going forward we want to understand much better how the drug works, and what other effects it has in animals.”

While the study of the GPER gene and it’s mechanisms in aging are still in the early stages of trials, the team says they do offer promising results.

Hannah Eisenberg is a news reporter at the Daily Lobo. She can be reached at or on Twitter @DailyLobo.