New study shows how tumor cells use mitochondria to keep growing

Hormone therapy is often used to treat prostate cancer that has spread to other parts of the body, but most patients develop resistance to hormone replacement therapy, making their disease more severe and possibly more fatal.

“One of the biggest challenges we face in the field is the majority prostate cancer Therapies target hormones — the androgen axis,” according to University of Colorado Cancer Center member Cecilia Caino, Ph.D. “But almost all patients develop resistance to those drugs and then develop additional disease that begins to move to other parts of the body. . It was reserved for the prostate, but can now move to the bones or liver, or lungs. This is definitely a big problem, because when you first start negotiating vital organsthe patient eventually dies.”

In the spring of 2021, Caino received an award from the U.S. Department of Defense design the Cancer Research Program to explore the role of mitochondria – the small energy industry in cells that help reduce food into fat – in the metastatic cancer of the prostate.

In the first study recently published in the journal Cancer ResearchCaino and her researchers discovered this cancer cells use mitochondria to control growth and identify pathogens that can damage tumors if left untreated. In addition to the Department of Defense, the American Cancer Society, the Boettcher Foundation, and the National Institutes of Health received funding for the study.

“We know that antidepressants are resistant to stress in general; this is what makes them so difficult to target with therapies, “said Caino. “But when the tumors grow rapidly, they begin to deplete the nutrients to keep building. They use this mitochondrial method we described to temporarily slow down, adjust, and expand their capacity to connect other blocks to build molecules.”

Something to be targeted

Caino and her team also found that yes mitochondrial protein the so-called MIRO2 is overreacting and straining in metastatic prostate cancer. Having previously discovered that MIRO2 interacts with two other proteins called GCN1 and GCN2 to help prostate cancer cells to withstand conditions that would inhibit normal cell proliferation, Caino now thinks that depleting this compound of proteins can inhibit the mitochondrial system which prevents tumor cells from destroying themselves by expanding rapidly.

“Our next step is to monitor the type of animals that have metastases and to see if we can eliminate cancer tumors or prevent the virus from occurring early,” she said. “We also learn a lot more about the complex, because we want to know how it is designed. This will help us to identify patients who will benefit from the treatment from those who cannot.”

Researchers will begin to treat metastasis with medications that are used to treat it acute lymphocytic leukemiabut Caino also hopes to eventually create a drug that will prevent the complex process from developing.

“Drugs often work for a while, then stop working. You have to think about what to do if this treatment doesn’t work anymore,” she said. “Hopefully we can come up with a strategy to stop the implementation of distance.”

Critical research

Caino is particularly excited about this research as it represents the first paper reviewed by her peers as a major author. He is also 22 years old from his first experience in lab research.

“I decided to start a new research line that did not originate directly from my undergraduate studies,” she said. “I also chose to start my lab with a group of two undergraduate students and a group of highly-skilled, highly-skilled, highly-skilled, highly-regarded, highly-skilled, highly-skilled, highly-skilled, highly-skilled, highly-skilled, highly-skilled, highly-skilled, highly-skilled, highly-skilled. a highly-skilled professional football team, where I invest in coaching while continuing to run the bench team myself. Walking this long, arduous journey has been a challenge and I have appealed to all the skills and abilities that I have.”