Interferon gamma inducible protein 16 (IFI16) expression is reduced in mantle cell lymphoma

Pier Paolo Piccaluga1,2,3, Mohsen Navari4,5,6, Axel Visani1

  • 1Department of Experimental, Diagnostic, and Specialty Medicine, University of Bologna, Bologna, Italy.

Heliyon
|December 17, 2019
PubMed

Insights

Interferon gamma (IFN)-inducible protein 16 (IFI16) expression is deregulated in mantle cell lymphoma (MCL). This deregulation impacts cell biology, but not patient survival in MCL.

Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Interferon gamma (IFN)-inducible protein 16 (IFI16) is part of the PYHIN-200 gene family and influences cell proliferation, survival, and differentiation.
  • IFI16 expression is regulated during B cell differentiation and has been investigated in B-cell chronic lymphocytic leukemia (B-CLL).

Purpose of the Study:

  • To compare IFI16 expression across various lymphomas, including Burkitt lymphoma, diffuse large B-cell lymphoma, follicular lymphoma, marginal zone lymphoma, and mantle cell lymphoma (MCL), against normal cell counterparts.
  • To investigate the association of IFI16 expression with cellular processes and patient survival in MCL.

Main Methods:

  • Quantitative analysis of IFI16 gene expression in different lymphoma subtypes and normal B cells.
  • Correlation analysis between IFI16 expression and genes involved in interferon response, cell cycle, apoptosis, proliferation, and metabolism.
  • Assessment of the relationship between IFI16 expression and patient survival in MCL.

Main Results:

  • IFI16 expression was significantly deregulated exclusively in mantle cell lymphoma (MCL) (p < 0.05).
  • IFI16 expression correlated with genes related to interferon response, cell cycle, cell death, proliferation, and notably, lipid and glucose metabolism.
  • No correlation was found between IFI16 expression and patient survival in the studied MCL cohort, despite MCL prognosis being linked to proliferation.

Conclusions:

  • IFI16 deregulation in MCL suggests potential alterations in cell biology, including metabolism and cell cycle regulation.
  • The complex relationship between IFI16 and MCL warrants further investigation, particularly concerning its role in disease pathogenesis and prognosis.
  • While IFI16 expression is altered in MCL, its direct impact on patient survival in this cohort was not evident, indicating a nuanced role.