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Applying an Inducible Expression System to Study Interference of Bacterial Virulence Factors with Intracellular Signaling
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Janus-faced bacterial regulation of epithelial cell death and survival: Association with colon carcinogenesis

Wei-Ting Kuo1, Tsung-Chun Lee2, Linda Chia-Hui Yu1

  • 1Graduate Institute of Physiology, National Taiwan University College of Medicine.

Molecular & Cellular Oncology
|June 17, 2016
PubMed

Insights

Lipopolysaccharide (LPS) signaling in the gut influences colon cancer. Toll-like receptor 4 (TLR4) on colon cells promotes cancer by resisting apoptosis triggered by CD14.

Area of Science:

  • Gastroenterology
  • Oncology
  • Immunology

Background:

  • Gut microbiota and lipopolysaccharide (LPS) signaling are implicated in colon cancer.
  • LPS receptor subunits on colonocytes play critical roles in tumorigenesis.

Purpose of the Study:

  • To investigate the distinct roles of LPS receptor subunits, toll-like receptor 4 (TLR4) and CD14, in colon cancer development.
  • To elucidate the mechanisms by which TLR4 and CD14 influence colonocyte apoptosis and epithelial-to-mesenchymal transition.

Main Methods:

  • Analysis of LPS receptor subunit expression in colonocytes.
  • Studies on the impact of TLR4 and CD14 on apoptosis induction.
  • Investigation of epithelial-to-cancer transition pathways.

Main Results:

  • Epithelial toll-like receptor 4 (TLR4) confers resistance to apoptosis.
  • TLR4 antagonizes the pro-apoptotic effects of its co-receptor CD14.
  • TLR4 activity contributes to the epithelial-to-cancer transition.

Conclusions:

  • TLR4 and CD14 exhibit opposing roles in colon cancer.
  • Targeting TLR4 may offer a therapeutic strategy for colon cancer by overcoming apoptosis resistance.
Keywords:
apoptosiscolorectal carcinomainnate immunityintestinal homeostasislipopolysaccharide

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