The protein, peroxisome proliferator-activated receptor delta (PPARD), normally helps cells burn fat for energy. In cancer cells, PPARD supports tumor growth. But researchers led by Assistant Professor Semir Beyaz found that activating the same protein in immune cells shifts the tumour environment in favour of the immune system.
"It's all about cell fitness," Beyaz said. "What cells eat affects who they are. When immune cells burn more fat, they become more fit for fighting cancer."
The team tested the approach on engineered immune cells known as CAR T cells, which are modified to recognise and attack cancer. When PPARD was activated in CAR T cells and tested against human colorectal cancer models, including miniature organoids grown from patient tissue and human tumours implanted in mice, tumour growth slowed or stopped.
The research could offer a new path for patients with difficult-to-treat colorectal cancer who have limited options after chemotherapy and newer immunotherapies fail. The work suggests that metabolic fitness of immune cells is a promising target for improving cancer treatments.
