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Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
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Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
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Oncogene-induced matrix reorganization controls CD8+ T cell function in the soft-tissue sarcoma microenvironment.

Ashley M Fuller1, Hawley C Pruitt2, Ying Liu1

  • 1Abramson Family Cancer Research Institute, Department of Pathology and Laboratory Medicine, Penn Sarcoma Program, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA.

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The transcriptional coactivator YAP1 drives collagen VI deposition, impairing CD8+ T cell function in sarcoma. Collagen I counteracts this, promoting anti-tumor immunity by supporting T cell function.

Keywords:
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Area of Science:

  • Immunology
  • Oncology
  • Cancer Biology

Background:

  • CD8+ T cell dysfunction limits antitumor immunity in solid tumors.
  • The tumor microenvironment's extracellular matrix (ECM) influences T cell function, but specific molecular impacts are unclear.
  • Dysregulated ECM deposition in tumors lacks well-defined upstream regulators.

Purpose of the Study:

  • To investigate how ECM composition affects CD8+ T cell function in undifferentiated pleomorphic sarcoma (UPS).
  • To identify upstream regulators of ECM deposition in the UPS tumor microenvironment (TME).

Main Methods:

  • Utilized an autochthonous murine model of UPS.
  • Analyzed data from multiple human patient cohorts.
  • Investigated the role of YAP1, collagen VI (COLVI), and collagen I (COLI) in the UPS TME.

Main Results:

  • YAP1 promotes COLVI deposition in the UPS TME.
  • COLVI inhibits CD8+ T cell function by remodeling collagen and impairing T cell autophagic flux, promoting immune evasion.
  • COLI counteracted COLVI's effects, enhancing CD8+ T cell function and acting as a tumor suppressor.

Conclusions:

  • Sarcoma CD8+ T cell responses are critically dependent on oncogene-driven ECM composition and remodeling.
  • YAP1-mediated COLVI deposition is a key mechanism of immune evasion in UPS.
  • Targeting ECM composition, specifically the balance of COLVI and COLI, may represent a therapeutic strategy to enhance antitumor immunity.