OR7A10 GPCR engineering boosts CAR-NK therapy against solid tumours

Nature

by Luojia Yang

February 26, 2026

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Researchers have discovered that engineering CAR-NK (chimeric antigen receptor-natural killer) cells with OR7A10, a G-protein-coupled receptor (GPCR), significantly enhances their effectiveness against solid tumors. In preclinical models, this modification improved CAR-NK cell proliferation, activation, cytotoxicity, and persistence in challenging tumor microenvironments. The study highlights that OR7A10-engineered cells showed superior anti-tumor activity, achieving complete tumor regression in 100% of mice with breast cancer. This breakthrough addresses key limitations of CAR-NK therapies, such as poor infiltration into tumors and resistance to the tumor environment. The research utilized cutting-edge CRISPR activation screens to identify OR7A10 as a "booster" that enhances NK cell functionality without requiring complex gene-editing techniques. By simply adding OR7A10 cDNA to CAR constructs, researchers achieved scalable and efficient improvements in CAR-NK performance. This approach simplifies manufacturing while maintaining therapeutic potency, making it a promising off-the-shelf solution for treating various solid tumors. The findings underscore the potential of targeting GPCRs like OR7A10 to unlock new therapeutic strategies for cancer immunotherapy. By overcoming exhaustion and improving functionality in primary human NK cells derived from diverse sources, this innovation brings CAR-NK therapies closer to clinical application. The study emphasizes the importance of identifying such "boosters" to enhance existing cell-based treatments and expand their utility against challenging cancers. This advancement matters because solid tumors remain a major challenge for cancer immunotherapy due to their ability to evade immune responses. By improving CAR-NK cells' ability to infiltrate, persist, and combat tumors, OR7A10 engineering could pave the way for more effective and scalable

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Originally published on Nature on 2/26/2026