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  • nrc
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  • tool
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  • Assistant Professor
  • Associate Professor
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  • Clinical Research Nurse
  • Clinician Researcher
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  • Master Student
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  • Permanent Researcher
  • Pharmacist
  • PhD Student
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  • Post-doc
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  • Project Manager
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  • Research Engineer
  • Retired scientist
  • Technician
  • Undergraduate Student
  • Veterinary
  • Visiting Scientist
  • Deputy Director of Center
  • Deputy Director of Department
  • Deputy Director of National Reference Center
  • Deputy Head of Facility
  • Director of Center
  • Director of Department
  • Director of Institute
  • Director of National Reference Center
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Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Science advances - 15 Apr 2022

Mastrogiovanni M, Vargas P, Rose T, Cuche C, Esposito E, Juzans M, Laude H, Schneider A, Bernard M, Goyard S, Renaudat C, Ungeheuer MN, Delon J, Alcover A, Di Bartolo V,

Link to Pubmed [PMID] – 35417240

Link to DOI – 10.1126/sciadv.abl5942

Sci Adv 2022 Apr; 8(15): eabl5942

Adenomatous polyposis coli (APC) is a tumor suppressor whose mutations underlie familial adenomatous polyposis (FAP) and colorectal cancer. Although its role in intestinal epithelial cells is well characterized, APC importance in T cell biology is ill defined. APC regulates cytoskeleton organization, cell polarity, and migration in various cell types. Here, we address whether APC plays a role in T lymphocyte migration. Using a series of cell biology tools, we unveiled that T cells from FAP patients carrying APC mutations display impaired adhesion and motility in constrained environments. We further dissected the cellular mechanisms underpinning these defects in APC-depleted CEM T cell line that recapitulate the phenotype observed in FAP T cells. We found that APC affects T cell motility by modulating integrin-dependent adhesion and cytoskeleton reorganization. Hence, APC mutations in FAP patients not only drive intestinal neoplasms but also impair T cell migration, potentially contributing to inefficient antitumor immunity.