DNA 'switch' uncovers new brake on breast cancer growth
· Medical Xpressedited by Sadie Harley, reviewed by Robert Egan
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Adelaide University researchers have found a DNA "switch" that helps the body stop the growth of the most common form of breast cancer, providing new insights that could help with future treatments. Up to 80% of breast cancer cases are classified as estrogen receptor-positive (ER+)—meaning their growth is driven by the hormone estrogen.
The research is published in the journal npj Breast Cancer.
Previous research has shown that another hormone receptor, the androgen receptor, can act as a tumor suppressor in ER+ breast cancer. Activating the androgen receptor has shown promise as a potential treatment strategy, but scientists are still working to understand exactly how it stops cancer cells from growing.
Researchers from Adelaide University's School of Medicine, the South Australian immunoGENomics Cancer Institute (SAiGENCI) and SAHMRI have now uncovered an important piece of that puzzle.
A DNA switch inside ZBTB16
The team had previously identified a gene called ZBTB16 as a possible contributor to this tumor-suppressing effect, with a higher presence of the gene linked to improved survival in patients with ER+ breast cancer.
However, this new study found that changing ZBTB16 levels in breast cancer cells did not alter the ability of the androgen receptor to suppress cell growth.
Instead, the researchers identified a small regulatory region of DNA hidden within the gene that proved to be critical.
"The surprising finding was that ZBTB16 itself was not responsible for the growth-suppressing effect," said Dr. Amy Dwyer from Adelaide University's School of Medicine.
"Instead, we found that a small DNA 'switch' sitting inside the gene helps the androgen receptor to restrain cancer cell growth."
This DNA "switch," known as HRRINT3, acts as an enhancer—a section of DNA that helps control gene activity. The androgen receptor binds to this enhancer when activated by androgens, hormones that are present in both women and men.
Deleting the switch weakened tumor suppression
Using CRISPR gene-editing technology, researchers deleted a small section of HRRINT3 to determine what would happen when the enhancer was removed.
"When we deleted this DNA 'switch,' the androgen receptor could no longer suppress breast cancer cell growth as effectively," said co-author Dr. Zeyad Nassar, a cancer researcher with Adelaide University's SAiGENCI and SAHMRI.
"We also observed broader disruption of androgen receptor signaling and increased activity of genes that drive cell division.
"This tells us that the enhancer is doing much more than simply controlling ZBTB16. It appears to be part of a wider regulatory network that helps the androgen receptor keep cancer cell proliferation in check."
Removing the DNA "switch" also led to a rapid increase in cell growth in other androgen receptor-positive breast and prostate cancer cell models, suggesting that it may have a broader role in restraining tumor growth across multiple androgen receptor-positive cancers.
Informing androgen receptor treatments
"This discovery gives us a new piece of the puzzle in understanding how the androgen receptor suppresses ER+ breast cancer," Dwyer said.
"Treatments that activate the androgen receptor are already being investigated for advanced ER+ breast cancer, so understanding the molecular machinery needed for this anticancer effect is important.
"Ultimately, this work could help us develop better ways to identify and treat patients with advanced disease who have stopped responding to hormone therapies."
The research is the result of a collaboration with researchers at the University of Bordeaux in France.
Publication details
Maliha Wajahat et al., A functional role for an intronic enhancer of ZBTB16 in AR-mediated tumour suppression in ER+ breast cancer, npj Breast Cancer (2026). DOI: 10.1038/s41523-026-01037-5
Journal information: npj Breast Cancer
Key medical concepts
androgen receptorER+ breast cancer
Clinical categories
OncologyClinical genetics Provided by University of Adelaide Who's behind this story?
Sadie Harley
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