Glutamine metabolic competition drives immunosuppressive reprogramming of intratumour GPR109A⁺ myeloid cells to promote liver cancer progression

Abstract

Our findings identify the immunometabolic crosstalk between liver cancer cells and myeloid cells facilitates tumour progression via a glutamine metabolism/ER stress/GPR109A axis, suggesting that GPR109A can be exploited as an immunometabolic checkpoint and putative target for cancer treatment.