SRC-3 gene elimination in immune cells triggers effective long-lasting anti-cancer response - Video

Published in the Proceedings of the National Academy of Sciences, recent study shows that in animal models of breast and prostate cancer, eliminating the gene SRC-3, specifically in a type of immune cell called regulatory T cells (Tregs), triggered a lifelong anti-cancer response that eradicated the tumor without the typical side effects observed with other therapies. Furthermore, transferring Tregs without SRC-3 to animals carrying breast cancer tumors also resulted in long-term elimination of the tumor without negative side effects.

SRC-3 is not only highly expressed in all human cancers and plays a role in cancer growth, but it is also strongly expressed in Tregs that regulate the immune response to cancer. Intrigued by the abundance of SRC-3 in Tregs and suspecting that it might play a role in controlling cancer progression.The research team generated mice lacking the SRC-3 gene only in Tregs (SRC-3 knock-out) and then compared breast cancer progression in these mice with the progression in mice that had the SRC-3 gene.

“We were surprised by the results,” said corresponding author Dr. Bert W. O’Malley. “Breast tumors were eradicated in the SRC-3 knock-outs. A subsequent injection of additional cancer cells in these mice did not give rise to new tumors, showing that there was no need to generate additional SRC-3 knock-outs to sustain tumor resistance. Importantly, transferring these cells to animals carrying pre-established breast tumors also resulted in cancer eradication. We obtained similar results with prostate cancer.”

The team also discovered that Tregs lacking SRC-3 mediated long-lasting tumor eradication by effectively modifying the environment surrounding the tumor into one that favored its elimination.

Reference:

Steroid receptor coactivator‑3 inhibition generates breast cancer antitumor immune microenvironment,Proceedings of the National Academy of Sciences,DOI 10.1073/pnas.2221707120,https://www.bcm.edu/news/