ArticleNature metabolism2020
Tumour-reprogrammed stromal BCAT1 fuels branched-chain ketoacid dependency in stromal-rich PDAC tumours.
Article in Nature metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers.
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Who cites it
128 citing papers in PubMed, 197 citations in OpenAlex.
- Remodeling of mitochondrial dynamics by metabolic pathways couples to oncogenic growth inScience advances · 2026Article
- Distinct metabolic dependency on BCAA defines cancer stemness and malignancy in human triple-negative breast cancer.Cell reports · 2026Article
- Immune-Metabolic Profiling Reveals Functional Heterogeneity Within Colorectal Cancer Consensus Molecular Subtypes.Biology · 2026Article
- Targeting the PARP10-BCAT2 axis disrupts branched-chain amino-acid metabolism to suppress bone metastasis in lung cancer.Cell death & disease · 2026Article
- Tumor-derived branched-chain α-keto acids activate Notch signaling in tumor-associated macrophages to limit immunity.Nature immunology · 2026Article
- MTFR2 promotes VDAC1 oligomerization to reprogram BCAA metabolism in tumor cells to polarize TAMs in LUAD.Cell death & disease · 2026Article
- BCAT1 inhibits glutamine-dependent Akt/mTOR signaling and nucleotide synthesis by initiating BTRC-mediated degradation of SLC3A2 in pancreatic adenocarcinoma.Cancer & metabolism · 2026Article
- Metabolic Salvage and Acyl-chain Remodeling Support Glycosphingolipid Synthesis within the PDAC Tumor Microenvironment.bioRxiv : the preprint server for biology · 2026Article
- Dietary intake and BCAA metabolism regulate pulmonary fibrosis through KDM4A-mediated epigenetic remodeling in male mice.Nature communications · 2026Article
- Reprogramming of nitrogen metabolism in tumors: mechanisms and therapeutic implications.Amino acids · 2026Review
- Integrative Analysis of Multiomic Pathways Predicts Cancer-Affected Lobes in Lung Cancer.Cancer prevention research (Philadelphia, Pa.) · 2026Article
- Pancreatic cancer-associated organ dysfunction promotes muscle autophagy and contributes to peripheral tissue wasting.bioRxiv : the preprint server for biology · 2026Article
- Cancer Metabolism and Its Historical & Molecular Foundations: An Overview.Drugs and drug candidates · 2026Article
- Metabolic characteristics in hepatocellular carcinoma: amino acid metabolic reprogramming.Molecular cancer · 2026Review
- Extracellular vesicles as modulators of cancer metabolism and microenvironment.Extracellular vesicles and circulating nucleic acids · 2026Review
- Branched-chain amino acid transaminases as promising targets in tumor therapy.Frontiers in cell and developmental biology · 2026Review
- Transcriptomic buffering detection: a computational approach to identifying essential gene dependencies in pancreatic cancer.Bioinformatics advances · 2026Article
- Harnessing the power of cancer-associated fibroblasts to revolutionize pancreatic cancer treatment.Cancer biology & medicine · 2025Review
- DDX6 undergoes phase separation to modulate metabolic plasticity and chemoresistance.Nature communications · 2025Article
- Integrated transcriptome and single-cell RNA sequencing analysis revealed the prognostic significance of GBP4 in pancreatic adenocarcinoma.Translational oncology · 2025Article
68 more citing papers are in PubMed but not listed here.
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Authors and funding
20 authors at 5 institutions in 1 country.
Funding
Abstract
Branched-chain amino acids (BCAAs) supply both carbon and nitrogen in pancreatic cancers, and increased levels of BCAAs have been associated with increased risk of pancreatic ductal adenocarcinomas (PDACs). It remains unclear, however, how stromal cells regulate BCAA metabolism in PDAC cells and how mutualistic determinants control BCAA metabolism in the tumour milieu. Here, we show distinct catabolic, oxidative and protein turnover fluxes between cancer-associated fibroblasts (CAFs) and cancer cells, and a marked reliance on branched-chain α-ketoacid (BCKA) in PDAC cells in stroma-rich tumours. We report that cancer-induced stromal reprogramming fuels this BCKA demand. The TGF-β-SMAD5 axis directly targets BCAT1 in CAFs and dictates internalization of the extracellular matrix from the tumour microenvironment to supply amino-acid precursors for BCKA secretion by CAFs. The in vitro results were corroborated with circulating tumour cells (CTCs) and PDAC tissue slices derived from people with PDAC. Our findings reveal therapeutically actionable targets in pancreatic stromal and cancer cells.
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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.