DNA ‘switch’ could offer new hope for breast cancer patients

A newly discovered DNA “switch” that helps halt the growth of breast cancer has opened new paths for treatment of the terrible disease.

In up to 80 per cent of breast cancer cases, tumour growth is driven by the hormone estrogen, and they called “estrogen receptor-positive” (ER+).

Previous research showed another hormone receptor, for androgen, can suppress tumour growth in these cancers, and scientists are researching how it can be used in treatment.

Now, Australian researchers from the Adelaide University School of Medicine, the South Australian ImmunoGENomics Cancer Institute, and South Australian Health and Medical Research Institute (SAHMRI), along with colleagues in France, have unlocked a key new finding.

The team had previously identified a gene called ZBTB16 as a possible contributor to this tumour-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.

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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,” Dr Amy Dwyer from Adelaide University’s School of Medicine said.

“Instead, we found that a small DNA ‘switch’ sitting inside the gene helps the androgen receptor to restrain cancer cell growth.”

Using gene-editing technology, the researchers deleted a small amount of the “switch” (technically a gene enhancer known as HRRINT3) to see what would happen when it was removed.

“When we deleted this DNA ‘switch’, the androgen receptor could no longer suppress breast cancer cell growth as effectively,” co-author Dr Zeyad Nassar, a cancer researcher with Adelaide University’s SAiGENCI and SAHMRI, said.

“We also observed broader disruption of androgen receptor signalling and increased activity of genes that drive cell division.”

He said this meant the “switch” appeared to be part of a wider regulatory network in the body that helped the androgen receptor keep a check on cancer cell growth.

Removing the “switch” also led to a rapid increase in other androgen receptor-positive breast and prostate cancer cell models, suggesting that it may have a broader role in restraining tumour growth in multiple cancers.

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The research has been published in the journal npj Breast Cancer and is the result of a collaboration with researchers at the University of Bordeaux in France.

“This discovery gives us a new piece of the puzzle in understanding how the androgen receptor suppresses ER+ breast cancer,” Dwyer said.

“Ultimately, this work could help us develop better ways to identify and treat patients with advanced disease who have stopped responding to hormone therapies.”