ArticleCell communication and signaling : CCS2024
1-Pyrroline-5-carboxylate inhibit T cell glycolysis in prostate cancer microenvironment by SHP1/PKM2/LDHB axis.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- Decoding the metabolic‑immune crosstalk: The role of glutamine and ammonium reprogramming in prostate cancer immune evasion (Review).Oncology reports · 2026Review
- The microbiome across the prostate disease continuum: from health and BPH to prostatitis/CPPS and cancer.Oncogene · 2026Review
- Construction of a survival model for predicting biochemical recurrence of prostate cancer based on propionate metabolism-related genes.Translational andrology and urology · 2026Article
- The proteostasis paradox: from systemic collapse in aging to pathway-specific addiction in prostate cancer.Frontiers in cell and developmental biology · 2026Review
- Uncovering the mediating role of CSF metabolites in the gut microbiota-glioblastoma axis via causal mediation analysis.Discover oncology · 2025Article
- Nanomedicines Targeting Metabolic Pathways in the Tumor Microenvironment: Future Perspectives and the Role of AI.Metabolites · 2025Review
- Lactate and lactylation in cancer.Signal transduction and targeted therapy · 2025Review
- Bibliometric analysis of glycolysis and prostate cancer research from 2004 to 2024.Discover oncology · 2025Article
- Epigenetic silencing of LDHB promotes hepatocellular carcinoma by remodeling the tumor microenvironment.Cancer immunology, immunotherapy : CII · 2024Article
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundOur previous studies demonstrated that 1-Pyrroline-5-carboxylate (P5C) released by prostate cancer cells inhibits T cell proliferation and function by increasing SHP1 expression. We designed this study to further explore the influence of P5C on T cell metabolism, and produced an antibody for targeting P5C to restore the functions of T cells.
methodWe co-immunoprecipated SHP1 from T cells and analyzed the proteins that were bound to it using liquid chromatography mass spectrometry (LC/MS-MS). The influence of P5C on T cells metabolism was also detected by LC/MS-MS. Seahorse XF96 analyzer was further used to identify the effect of P5C on T cells glycolysis. We subsequently designed and produced an antibody for targeting P5C by monoclonal technique and verified its effectiveness to restore the function of T cells in vitro and in vivo.
resultPKM2 and LDHB bind SHP1 in T cells, and P5C could increase the levels of p-PKM2 while having no effect on the levels of PKM2 and LDHB. We further found that P5C influences T cell energy metabolism and carbohydrate metabolism. P5C also inhibits the activity of PKM2 and decreases the content of intracellular lactic acid while increasing the activity of LDH. Using seahorse XF96 analyzer, we confirmed that P5C remarkably inhibits glycolysis in T cells. We produced an antibody for targeting P5C by monoclonal technique and verified that the antibody could oppose the influence of P5C to restore the process of glycolysis and function in T cells. Meanwhile, the antibody also inhibits the growth of prostate tumors in an animal model.
conclusionOur study revealed that P5C inhibits the process of glycolysis in T cells by targeting SHP1/PKM2/LDHB complexes. Moreover, it is important that the antibody for targeting P5C could restore the function of T cells and inhibit the growth of prostate tumors.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.