Glucose metabolism involved in PD-L1-mediated immune escape in the malignant kidney tumour microenvironment

Yongbo Yu1,2, Ye Liang2, Dan Li2

  • 1Department of Urology, The Affiliated Hospital of Qingdao University, Qingdao, 266003, China.

Cell Death Discovery
|January 19, 2021
PubMed

Insights

Glucose deficiency increases PD-L1 expression in renal cancer cells via the EGFR/ERK/c-Jun pathway. This elevated PD-L1 then enhances glycolysis, suggesting a novel therapeutic target for renal cell carcinoma (RCC).

Area of Science:

  • Cancer Biology
  • Metabolic Regulation
  • Immunotherapy

Background:

  • Programmed death receptor-ligand 1 (PD-L1) is vital for tumor immune evasion.
  • Tumor cells rely on glycolysis for energy, but its link to PD-L1 is unclear.
  • Understanding this relationship may reveal new therapeutic strategies for renal cell carcinoma (RCC).

Purpose of the Study:

  • To investigate the impact of glucose metabolism on PD-L1 expression in renal carcinoma.
  • To elucidate the signaling pathways involved in glucose-regulated PD-L1.
  • To explore the reciprocal regulation between PD-L1 and glycolysis in RCC.

Main Methods:

  • Assessed PD-L1 and epidermal growth factor receptor (EGFR) expression in 786-O and OS-RC-2 renal cancer cells under glucose deficiency and recovery.
  • Utilized EGFR and extracellular regulated protein kinases 1 and 2 (ERK1/2) inhibitors to probe signaling pathways.
  • Investigated the role of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3) in mediating glycolysis.

Main Results:

  • Glucose deficiency upregulated PD-L1 expression in both renal cancer cell lines.
  • EGFR signaling, through the EGFR/ERK/c-Jun pathway, mediated glucose-deficiency-induced PD-L1 upregulation.
  • Elevated PD-L1 expression promoted glycolysis by upregulating PFKFB3.

Conclusions:

  • Glucose metabolism critically influences PD-L1 expression in renal cancer via the EGFR/ERK/c-Jun axis.
  • PD-L1 reciprocally regulates glycolysis, enhancing it under adverse conditions.
  • The interplay between glucose metabolism and PD-L1 presents a promising multi-target therapeutic avenue for RCC.

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