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SIRT5 Contributes to Colorectal Cancer Growth by Regulating T Cell Activity

Ke Wang1, Zuojian Hu2, Cuiping Zhang1,3

  • 1Institutes of Biomedical Sciences & Minhang Hospital, Shanghai Medical College, Fudan University, Shanghai 200032, China.

Journal of Immunology Research
|September 21, 2020
PubMed

Insights

Mice lacking SIRT5 resist colorectal cancer development by enhancing T cell responses and increasing anti-tumor immunity. This study reveals SIRT5

Area of Science:

  • Immunology
  • Oncology
  • Biochemistry

Background:

  • Sirtuin 5 (SIRT5) is recognized for its role in metabolic regulation.
  • The specific function of SIRT5 in tumorigenesis, particularly its influence on the tumor microenvironment, remains largely uncharacterized.

Purpose of the Study:

  • To investigate the role of SIRT5 in colitis-associated colorectal tumorigenesis.
  • To elucidate the mechanisms by which SIRT5 affects the tumor microenvironment and immune cell function.

Main Methods:

  • Utilized knockout mouse models (Sirt5-/-) subjected to AOM/DSS induction for colitis-associated colorectal cancer.
  • Performed proteomic and network analyses to identify molecular pathways affected by SIRT5.
  • Assessed T cell activation, differentiation of CD4+ regulatory T (Treg) cells, and T helper 1 (Th1) cells.

Main Results:

  • Sirt5 knockout mice exhibited resistance to AOM/DSS-induced colorectal tumorigenesis.
  • Elevated levels of interferon-gamma (IFN-γ) were observed in the tumor microenvironment of Sirt5 knockout mice.
  • SIRT5 deficiency led to enhanced T cell activation and altered differentiation of Treg and Th1 cells, impacting the balance of immune cells.

Conclusions:

  • SIRT5 plays a critical role in regulating T cell activation and differentiation.
  • The balance between immunosuppressive Treg cells and inflammatory Th1 cells, influenced by SIRT5, is crucial in colon cancer development.
  • SIRT5 emerges as a key regulator in colorectal tumorigenesis through its modulation of the tumor immune microenvironment.

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