Nature Communications (Aug 2019)

CAF hierarchy driven by pancreatic cancer cell p53-status creates a pro-metastatic and chemoresistant environment via perlecan

  • Claire Vennin,
  • Pauline Mélénec,
  • Romain Rouet,
  • Max Nobis,
  • Aurélie S. Cazet,
  • Kendelle J. Murphy,
  • David Herrmann,
  • Daniel A. Reed,
  • Morghan C. Lucas,
  • Sean C. Warren,
  • Zehra Elgundi,
  • Mark Pinese,
  • Gabriella Kalna,
  • Daniel Roden,
  • Monisha Samuel,
  • Anaiis Zaratzian,
  • Shane T. Grey,
  • Andrew Da Silva,
  • Wilfred Leung,
  • Australian Pancreatic Genome Initiative (APGI),
  • Suresh Mathivanan,
  • Yingxiao Wang,
  • Anthony W. Braithwaite,
  • Daniel Christ,
  • Ales Benda,
  • Ashleigh Parkin,
  • Phoebe A. Phillips,
  • John M. Whitelock,
  • Anthony J. Gill,
  • Owen J. Sansom,
  • David R. Croucher,
  • Benjamin L. Parker,
  • Marina Pajic,
  • Jennifer P. Morton,
  • Thomas R. Cox,
  • Paul Timpson

DOI
https://doi.org/10.1038/s41467-019-10968-6
Journal volume & issue
Vol. 10, no. 1
pp. 1 – 22

Abstract

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Subtypes of cancer associated fibroblasts can both promote and suppress tumorigenesis. Here, the authors investigate how p53 status in pancreatic cancer cells affects their interaction with cancer associated fibroblasts, and report perlecan as a mediator of the pro-metastatic environment.