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IFN-α/β-mediated NK2R expression is related to the malignancy of colon cancer cells

Huihui Xiang1,2, Yujiro Toyoshima1,2, Weidong Shen1

  • 1Division of Functional Immunology, Section of Disease Control, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan.

Cancer Science
|May 13, 2022
PubMed

Insights

High NK2R gene expression correlates with poor survival in colorectal cancer. Interferon stimulation boosts NK2R in colon cancer cells, suggesting NK2R blockade as a potential therapeutic strategy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Neurokinin 2 receptor (NK2R) is a G protein-coupled receptor involved in various physiological processes.
  • The role and regulation of NK2R in cancer cells, particularly colorectal cancer, remain incompletely understood.

Purpose of the Study:

  • To investigate the role of NK2R in colorectal cancer progression.
  • To explore the regulation of NK2R expression by Interferon (IFN-α/β) in colon cancer cells.
  • To evaluate the therapeutic potential of NK2R blockade in colon cancer.

Main Methods:

  • Correlation analysis of NK2R gene expression with patient survival data.
  • Investigated the effect of IFN-α/β on NK2R expression in colon cancer cells using Janus kinase 1/2 (JAK 1/2) pathway inhibitors.
  • Assessed the impact of Neurokinin A (NKA) stimulation and NK2R antagonist on cancer cell proliferation and signaling pathways (ERK1/2).
  • Evaluated the efficacy of NK2R antagonist in preclinical mouse models (CT26-bearing mice) with or without polyinosinic-polycytidylic acid.
  • Examined the effect of NK2R overexpression on tumor growth and metastasis in mice.

Main Results:

  • High NK2R gene expression is linked to poorer survival in colorectal cancer patients.
  • IFN-α/β significantly increases NK2R gene expression in colon cancer cells via the JAK 1/2 pathway.
  • NKA stimulation enhances proliferation and ERK1/2 phosphorylation in IFN-α/β-treated colon cancer cells.
  • NK2R blockade reduces colon cancer cell proliferation in vitro.
  • NK2R antagonist administration suppresses tumor growth and metastasis in vivo.
  • Overexpression of NK2R in cancer cells promotes tumorigenesis and metastatic colonization.

Conclusions:

  • IFN-α/β-mediated NK2R expression contributes to colon cancer malignancy.
  • NK2R blockade represents a potential therapeutic strategy for colon cancer treatment.
Keywords:
JAKcolon cancermalignancyneurokinin-2 receptortype I IFN

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