Members of Professor Zheng Ji’s research team discuss the study at Xinqiao Hospital in Chongqing, southwest China. (Photo/ Shangyou News)

Chongqing - On August 17, researchers from Chongqing’s Xinqiao Hospital and China Pharmaceutical University reported a potential new prostate cancer treatment in Advanced Materials that turns immunologically “cold” tumors into “hot” ones.

On August 17, researchers from Chongqing's Xinqiao Hospital and China Pharmaceutical University reported in Advanced Materials a potential prostate cancer treatment that turns "cold" tumors "hot." (Screenshot/ Advanced Materials)

The teams, led by Professor Zheng Ji of Xinqiao Hospital’s Urology Center and Professor Zhong Wenying of China Pharmaceutical University, focused on prostate cancer’s resistance to immunotherapy. 

Unlike tumors that respond well to such treatment, prostate cancer is typically immunologically “cold,” with limited immune-cell infiltration and activation, making improved treatment sensitivity a longstanding clinical challenge.

At the heart of the research is a strategy to turn "cold" tumors into "hot" tumors. To address this challenge, the team focused on lysosomes, cellular organelles found within cancer cells.

If a cell is like a city, the lysosome is like a waste disposal and recycling center, responsible for breaking down and recycling center. Once the lysosomal structure is disrupted, its contents are released, which can damage tumor cells.

The team constructed a supramolecular nanoplatform that accumulates in lysosomes and reassembles after entering prostate tumor cells, prolonging the retention of the therapeutic material within the cells. 

The platform also uses ultrasound as an external stimulus. When the tumor site is exposed to ultrasound, the platform is activated to produce cytotoxic substances that disrupt the lysosomal membrane, triggering tumor cell death .

Killing tumor cells is only the first step. The ultimate goal is to activate the body's own antitumor immunity. Rather than simply killing tumor cells, the team aims to harness tumor cell death to stimulate the body's own antitumor immune response.

The research shows that combining lysosomal disruption with an immunostimulating approach can turn the "cold" tumors into "hot" tumors. Ultrasound-induced lysosomal disruption triggers tumor cell death and the release of damage-associated molecular patterns. 

These signals, in turn, activate a specific signaling pathway that amplifies the immune response, promotes the maturation of antigen-presenting cells, and enhances T cell-mediated antitumor immune responses.

The research provides a new strategy for improving the limited efficacy of prostate cancer treatment and lays a theoretical and experimental foundation for treating other "cold" tumors.

(Li Jiayan, as an intern, also contributed to this report.)