4.1 Article

Mast cell modulates tumorigenesis caused by repeated bowel inflammation condition in azoxymethane/dextran sodium sulfate-induced colon cancer mouse model

Journal

BIOCHEMISTRY AND BIOPHYSICS REPORTS
Volume 30, Issue -, Pages -

Publisher

ELSEVIER
DOI: 10.1016/j.bbrep.2022.101253

Keywords

Colitis; Colorectal carcinoma; Dextran sodium sulfate; Mast cells; Tumorigenesis; Inflammation

Funding

  1. National Research Foundation of Korea (NRF) - Korea government (MSIT) [2019R1F1A1061198]
  2. BK21FOUR 21st Century of Medical Science Creative Human Resource Development Center
  3. National Research Foundation of Korea [2019R1F1A1061198] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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Mast cells play an important role in the development and growth of colon cancer by regulating pro-inflammatory cytokines and inflammatory mediators.
Mast cells infiltrate the inflammatory microenvironment and regulate the production of many pro-inflammatory cytokines and mediators of inflammatory cell production to promote tumor development and growth in intestinal lesions. Currently, there are insufficient studies of the mediators and signaling pathways regulated by mast cells that influence the pathogenesis of colon cancer in inflamed colon tissue. This study aimed to confirm the role of mast cells in the incidence and growth of colitis-associated colon cancer (CAC) and to identify inflammationmediated factors and signaling pathways related to tumor development. CAC was induced by the administration of azoxymethane (AOM) and dextran sodium sulfate (DSS) in mast cell-deficient (WBB6F1/J-W/WV) and mast cell-sufficient control (WBB6F1_+/+) mice. The results confirmed that mast cell-deficient mice exhibited less tumor formation than normal mice under the same conditions, and down-regulated expression of proinflammatory cytokines and mediators. Mast cells play an important role in tumor formation by regulating pro-inflammatory cytokines and inflammatory mediators in CAC, indicating that they can act as new targets for the prevention and treatment of CAC.

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