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Updated: Jun 21, 2026

In vitro Organoid Culture of Primary Mouse Colon Tumors
07:33

In vitro Organoid Culture of Primary Mouse Colon Tumors

Published on: May 17, 2013

Toll-like receptor 4 activation increases Akt phosphorylation in colon cancer cells

Hung Q Doan1, Kanika A Bowen, Lindsey A Jackson

  • 1Department of Surgery, The University of Texas Medical Branch, Galveston, TX, USA.

Anticancer Research
|July 15, 2009
PubMed
Abstract

Insights

Toll-like receptor 4 (TLR4) is overexpressed in colorectal cancer (CRC). Activating TLR4 with lipopolysaccharide (LPS) stimulates the PI3K/Akt pathway, suggesting TLR4 as a potential therapeutic target for CRC.

Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Toll-like receptors (TLRs) are key components of innate immunity.
  • Overexpression of TLRs is linked to various cancers, including colorectal cancer (CRC).
  • The phosphatidylinositol-3'-kinase (PI3K)/Akt pathway is crucial for CRC growth and progression.

Purpose of the Study:

  • To investigate TLR4 signaling in human colorectal cancers.
  • To determine if the PI3K/Akt pathway is activated in CRC.
  • To explore the relationship between TLR4 and PI3K/Akt activation in CRC.

Main Methods:

  • Human CRC tissues and adjacent normal mucosa were analyzed for TLR4 expression.
  • CRC cell lines were treated with lipopolysaccharide (LPS), a TLR4 ligand.
  • Akt phosphorylation was measured to assess PI3K/Akt pathway activation.

Main Results:

  • Human CRCs exhibited significantly higher TLR4 expression compared to normal adjacent mucosa.
  • TLR4 was detected in CRC cells.
  • LPS treatment led to a time-dependent increase in Akt phosphorylation in TLR4-positive CRCs.

Conclusions:

  • TLR4 is expressed in human colorectal cancers.
  • TLR4 activation by LPS leads to PI3K/Akt pathway activation.
  • Targeting TLR4 may represent a novel therapeutic strategy for colorectal cancer.

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