A Cancer Cell-Intrinsic GOT2-PPARδ Axis Suppresses Antitumor Immunity.
Jaime AbregoHannah Sanford-CraneChet OonXu XiaoCourtney B BettsDuanchen SunShanthi NagarajanLuis DiazHolly SandborgSohinee BhattacharyyaZheng XiaLisa M CoussensPeter TontonozMara H ShermanPublished in: Cancer discovery (2022)
Prior studies demonstrate the important moonlighting functions of metabolic enzymes in cancer. We find that the mitochondrial transaminase GOT2 binds directly to fatty acid ligands that regulate the nuclear receptor PPARδ, and this functional interaction critically regulates the immune microenvironment of pancreatic cancer to promote tumor progression. See related commentary by Nwosu and di Magliano, p. 2237.. This article is highlighted in the In This Issue feature, p. 2221.
Keyphrases
- fatty acid
- papillary thyroid
- insulin resistance
- stem cells
- oxidative stress
- squamous cell
- machine learning
- signaling pathway
- deep learning
- case control
- biofilm formation
- metabolic syndrome
- skeletal muscle
- squamous cell carcinoma
- type diabetes
- childhood cancer
- binding protein
- young adults
- adipose tissue
- candida albicans