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The overexpression of Tipe2 in CRC cells suppresses survival while endogenous Tipe2 accelerates AOM/DSS induced-tumor

Yan Li1,2, Na Zhang1, Chao Ma3

  • 1Key Laboratory of Infection and Immunity of Shandong Province, Department of Immunology, Shandong University School of Basic Medical Science, Jinan, Shandong, China.

Cell Death & Disease
|October 27, 2021
PubMed

Insights

Tumor Protein p73 (Tipe2) has a dual role in aging and cancer. Overexpressed Tipe2 can suppress cancer cell growth, but its natural presence may promote tumor initiation in inflammatory conditions.

Area of Science:

  • Immunology
  • Oncology
  • Aging Research

Background:

  • Aging increases cancer risk, but mechanisms remain unclear.
  • TNFAIP8L2 (Tipe2) regulates homeostasis by inhibiting TLR and TCR signaling.
  • Tipe2's role in senescence and cancer is under investigation.

Purpose of the Study:

  • To investigate the dual function of Tipe2 in regulating senescence and tumorigenesis.
  • To explore Tipe2's impact on age-related diseases like colorectal cancer (CRC).

Main Methods:

  • Overexpression of Tipe2 in CRC cells and assessment of senescence.
  • Analysis of Tipe2 knockout (KO) mice treated with D-Galactose (D-Gal).
  • Evaluation of AOM/DSS-induced CRC initiation in Tipe2 KO mice.
  • Investigating the role of regulatory T cells (Treg) and CD25.

Main Results:

  • Tipe2 overexpression induces senescence in CRC cells, inhibiting telomerase activity.
  • Tipe2 KO mice showed a less severe CD4:CD8 ratio inversion and lower Treg percentages after D-Gal treatment.
  • Tipe2 KO mice were more tolerant to AOM/DSS-induced CRC, with reduced Treg levels within intraepithelial lymphocytes (IEL).
  • Antibodies against CD25 ameliorated tumorigenesis.

Conclusions:

  • Overexpressed Tipe2 suppresses tumor cell proliferation and survival.
  • Endogenous Tipe2 promotes tumorigenesis initiation in inflammatory environments, partly via Treg modulation.

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