Targeting the mitochondrial pathway may be a potential strategy to stop prostate cancer growth

Targeting the mitochondrial pathway may be a potential strategy to stop prostate cancer growth

Hormone therapy is often used to treat prostate cancer that has spread to other parts of the body, but many patients develop resistance to hormone therapy, causing their disease to become more aggressive and possibly more deadly.

“One of the big challenges we face in this field is that the majority of prostate cancer treatments target the hormone-;androgen axis,” says University of Colorado Cancer Center member Cecilia Caino, Ph.D. “But almost all patients develop resistance to these drugs and then develop a more serious disease that starts to spread to other parts of the body. It used to be in the prostate, but it can now travel to the bones or the liver or the lungs. That’s a really big problem, because when you start to do damage With vital organs, the patient will eventually die.”

In the spring of 2021 Caino received an Idea Award from the US Department of Defense Cancer Research Program for an investigation of the role of mitochondria; small energy factories in cells that help break down food into fuel -; In metastatic prostate cancer.

In a preliminary research published recently in the journal Molecular Cancer ResearchKaino and her fellow investigators discovered that cancer cells use mitochondria to control their growth and detect stress that can destroy a tumor cell if not controlled. In addition to the Department of Defense, the research is funded by the American Cancer Society, the Boettcher Foundation, and the National Institute of General Medical Sciences.

“We know that cancer cells are very resistant to stress in general; that’s what makes them very difficult to target with therapies,” Kaino says. “But when tumors grow too fast, they start to run out of nutrients to keep building. They use the mitochondrial pathway we’re describing to slow down their speed for a moment, adapt, and expand their ability to make more mass to build cells.”

Compound for targeting

Kino and her team also found that a mitochondrial protein called MIRO2 is overexpressed in metastatic prostate cancer tumors. Having previously found that MIRO2 works with two other proteins called GCN1 and GCN2 to help metastatic prostate cancer cells withstand conditions in which normal cell growth is inhibited, Caino now hypothesizes that targeting this protein complex could suppress the mitochondrial process that prevents cancer cells from destroying themselves During the expansion very quickly.

“Our next step is to treat animal models that have had metastases and see if we can eliminate the tumor or prevent metastases from occurring in the first place,” she says. “We also learn a lot about the complex, because we want to know how it is regulated. This will help us divide the patients who will benefit from the treatment from those who will not.”

Researchers will begin treating the malignancy with an existing drug used to treat acute lymphocytic leukemia, but Kaino also hopes to eventually design a drug that prevents the compound from forming in the first place.

“Often the drugs work for a while, and then they stop working. You really have to think about what you’re going to do when that drug isn’t working anymore,” she says. “Hopefully we can come up with a strategy to stop the process further upstream.”

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Kino is particularly excited about this research as it represents the first peer-reviewed paper as a high-profile interview author. It also marks 22 years of her first lab research experience.

“I decided to start a new path of research that did not stem directly from my postdocs,” she says. “I also chose to start my lab with a couple of graduate students and a technician, investing in their training while still getting involved in the bench work myself. Walking this long, winding road was challenging and required every skill and strength I had.”

source:

University of Colorado Anschutz

Journal reference:

10.1158 / 1541-7786.MCR-21-0374

2022-05-11 01:50:00

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