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Pancreatic stellate cells support tumour metabolism through autophagic alanine secretion

Author

Listed:
  • Cristovão M. Sousa

    (Dana-Farber Cancer Institute, Harvard Medical School)

  • Douglas E. Biancur

    (Dana-Farber Cancer Institute, Harvard Medical School)

  • Xiaoxu Wang

    (Dana-Farber Cancer Institute, Harvard Medical School)

  • Christopher J. Halbrook

    (University of Michigan Medical School)

  • Mara H. Sherman

    (Gene Expression Laboratory, Howard Hughes Medical Institute, The Salk Institute for Biological Studies)

  • Li Zhang

    (University of Michigan Medical School)

  • Daniel Kremer

    (University of Michigan Medical School)

  • Rosa F. Hwang

    (The University of Texas M.D. Anderson Cancer Center)

  • Agnes K. Witkiewicz

    (UT Southwestern
    Simmons Cancer Center, UT Southwestern)

  • Haoqiang Ying

    (UT MD Anderson Cancer Center)

  • John M. Asara

    (Beth Israel Deaconess Medical Center and Harvard Medical School)

  • Ronald M. Evans

    (Gene Expression Laboratory, Howard Hughes Medical Institute, The Salk Institute for Biological Studies)

  • Lewis C. Cantley

    (Meyer Cancer Center, Weill Cornell Medical College)

  • Costas A. Lyssiotis

    (University of Michigan Medical School
    University of Michigan Medical School)

  • Alec C. Kimmelman

    (Dana-Farber Cancer Institute, Harvard Medical School
    †Present Address: Department of Radiation Oncology, Perlmutter Cancer Center, NYU Langone Medical Center, New York, New York 10016, USA.)

Abstract

Pancreatic adenocarcinoma cells drive autophagy in tumour microenvironment-associated stellate cells, which release alanine that is used by the cancer cells as a carbon source for a variety of metabolic processes in an otherwise nutrient-poor environment.

Suggested Citation

  • Cristovão M. Sousa & Douglas E. Biancur & Xiaoxu Wang & Christopher J. Halbrook & Mara H. Sherman & Li Zhang & Daniel Kremer & Rosa F. Hwang & Agnes K. Witkiewicz & Haoqiang Ying & John M. Asara & Ron, 2016. "Pancreatic stellate cells support tumour metabolism through autophagic alanine secretion," Nature, Nature, vol. 536(7617), pages 479-483, August.
    • Handle: RePEc:nat:nature:v:536:y:2016:i:7617:d:10.1038_nature19084
    DOI: 10.1038/nature19084
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    Cited by:

    1. Yuying Tan & Junjie Li & Guangyuan Zhao & Kai-Chih Huang & Horacio Cardenas & Yinu Wang & Daniela Matei & Ji-Xin Cheng, 2022. "Metabolic reprogramming from glycolysis to fatty acid uptake and beta-oxidation in platinum-resistant cancer cells," Nature Communications, Nature, vol. 13(1), pages 1-16, December.
    2. Xianbing Zhu & Zheng Fu & Shary Y. Chen & Dionzie Ong & Giulio Aceto & Rebecca Ho & Jutta Steinberger & Anie Monast & Virginie Pilon & Eunice Li & Monica Ta & Kyle Ching & Bianca N. Adams & Gian L. Ne, 2023. "Alanine supplementation exploits glutamine dependency induced by SMARCA4/2-loss," Nature Communications, Nature, vol. 14(1), pages 1-16, December.
    3. Nneka E. Mbah & Amy L. Myers & Peter Sajjakulnukit & Chan Chung & Joyce K. Thompson & Hanna S. Hong & Heather Giza & Derek Dang & Zeribe C. Nwosu & Mengrou Shan & Stefan R. Sweha & Daniella D. Maydan , 2024. "Therapeutic targeting of differentiation-state dependent metabolic vulnerabilities in diffuse midline glioma," Nature Communications, Nature, vol. 15(1), pages 1-21, December.
    4. Ali Vaziri-Gohar & Jonathan J. Hue & Ata Abbas & Hallie J. Graor & Omid Hajihassani & Mehrdad Zarei & George Titomihelakis & John Feczko & Moeez Rathore & Sylwia Chelstowska & Alexander W. Loftus & Ru, 2023. "Increased glucose availability sensitizes pancreatic cancer to chemotherapy," Nature Communications, Nature, vol. 14(1), pages 1-13, December.

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