New research may lead to better treatment of prostate, ovarian, and breast cancer

May 21, 2021

Researchers at the UVA Cancer Center have revealed important new insights into how a hormone called androgen acts on cells. This finding may support efforts to develop better treatments for prostate, ovarian, and breast cancer.

Bryce M in the Department of Biochemistry and Molecular Genetics. Dr. Paschal has uncovered a new mechanism for how androgen hormones regulate communication within prostate cancer cells. Image Credit: UVA Cancer Center

This finding reveals how androgens interact with intracellular receptors to affect gene activity. This process is important for both healthy cells and certain cancers. For example, hormone therapy for prostate cancer aims to reduce the amount of androgens in the body or prevent androgens from fueling cancer cells. However, this approach does not work for some men and ultimately fails for others. That’s why scientists are keen to better understand how our cells and cancer interact with androgens.

“Our research reveals a new mechanism for how androgens regulate communication within prostate cancer cells,” said Dr. Bryce M. Pascal, Department of Biochemistry and Molecular Genetics, UVA School of Medicine. Says. “Anti-androgens continue to be the cornerstone of prostate cancer treatment. The more we understand how androgens work, the more clinicians design why androgens fail and better treatments. You will be able to understand how. “

Androgens and cancer

In a new paper in the scientific journal Nature Communications, Paschal and his colleagues explain how complex signaling systems regulate androgen receptor activity. The system they discovered uses “writers” and “readers” to modify cellular proteins. It’s like how a computer reads and writes information.

Scientists recognize the importance of these modified proteins, but it has been difficult to understand how they affect androgen receptors. One key to the regulatory process discovered by Paschal and his SOM team is PARP7 gene. Parp7 is part of a family of enzymes involved in important cellular functions, including DNA repair.

Certain anti-cancer drugs already target certain Parp enzymes. These drugs are used to treat prostate, ovarian, and breast cancer in patients with mutations in DNA repair genes. Androgens are usually discussed in the context of prostate cancer, but androgens can also be important in ovarian and breast cancer.

Paschal’s new discoveries may provide fresh insights into these Parp medications and lead to improved treatments that help patients get the best results. In addition, Paschal and his team found low levels of Parp7 in prostate cancer that has spread to other parts of the body than the original tumor. It may suggest that a decrease in Parp7 is associated with disease progression, researchers say.

Paschal and his colleagues, with new androgen insights, have provided scientists with important new directions for exploring in the fight against prostate and other cancers.

The next step is to use a preclinical model to determine the role this pathway plays in the progression of prostate cancer and whether inhibition of the pathway delays the disease. I am very excited about what I have learned so far. Our research emphasizes that there is still much to learn and that basic science plays an important role in defining the molecular background of enzymes and drug action. “”

Dr. Bryce M. Pascal, Department of Biochemistry and Molecular Genetics, UVA School of Medicine

About research

Research teams include Chun-Song Yang, Kasey Jividen, Teddy Kamata, Natalia Dworak, Luke Oostdyk, Bartlomiej Remlein, Yasin Pourfarjam, In-Kwon Kim, Kang-Ping Du, Tarek Abbas, Nicholas E. Sherman, David Wotton, Paschal. It was configured. ..

This work was supported by the National Cancer Institute, National Cancer Institute Grant CA214872.

Source:

Journal reference:

Yang, C-.S. , et al. (2021) Androgen signaling regulates the assembly of protein complexes using writers and readers of ADP ribosylation. Nature Communications.. doi.org/10.1038/s41467-021-23055-6..

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