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

Yang YangTianduo PeiChaobao LiuMingtao CaoXiaolin HuJie YuanFengqian ChenBao GuoYuemei HongJibin LiuBin LiXiaoguang LiHui Wang
Published in: Gut (2024)
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.
Keyphrases
  • induced apoptosis
  • cell cycle arrest
  • fatty acid
  • bone marrow
  • dendritic cells
  • acute myeloid leukemia
  • endoplasmic reticulum stress
  • dna damage
  • oxidative stress
  • cell death
  • signaling pathway
  • pi k akt