Related Experiment Video

Updated: Aug 15, 2026

An Immunofluorescent Method for Characterization of Barrett’s Esophagus Cells
08:54

An Immunofluorescent Method for Characterization of Barrett’s Esophagus Cells

Published on: July 20, 2014

beta-Catenin-mediated signaling: a novel molecular target for chemoprevention with anti-inflammatory substances

Joydeb Kumar Kundu1, Kang-Yell Choi, Young-Joon Surh

  • 1National Research Laboratory of Molecular Carcinogenesis and Chemoprevention, College of Pharmacy, Seoul National University, Shinlim-dong, Kwanak-ku, Seoul 151-742, South Korea.

Biochimica Et Biophysica Acta
|October 18, 2005
PubMed

Insights

Inflammation contributes to cancer development. This review explores how anti-inflammatory drugs and phytochemicals may prevent cancer by targeting beta-catenin signaling pathways involved in carcinogenesis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Inflammation is increasingly recognized as a key factor in cancer development and progression.
  • Anti-inflammatory substances show promise for cancer chemoprevention.
  • Cyclooxygenase-2 (COX-2) is a known molecular target for anti-inflammatory chemoprevention.

Purpose of the Study:

  • To review the role of beta-catenin-mediated signaling in linking inflammation and cancer.
  • To explore the potential of modulating beta-catenin signaling for cancer chemoprevention.
  • To examine the effects of nonsteroidal anti-inflammatory drugs (NSAIDs) and phytochemicals on this pathway.

Main Methods:

  • Literature review of clinical and laboratory-based studies.
  • Analysis of cellular and molecular biology research on signaling cascades.
  • Focus on beta-catenin pathways in relation to carcinogenesis.

Main Results:

  • Beta-catenin-mediated signaling is suggested as a potential link between inflammation and cancer.
  • NSAIDs and anti-inflammatory phytochemicals may modulate inappropriately activated beta-catenin signaling.
  • Further elucidation of these signaling mechanisms is needed for effective chemoprevention strategies.

Conclusions:

  • Targeting beta-catenin signaling pathways offers a promising avenue for cancer chemoprevention.
  • Anti-inflammatory agents, including NSAIDs and phytochemicals, warrant further investigation for their role in modulating these pathways.
  • Understanding the interplay between inflammation, beta-catenin, and carcinogenesis is crucial for developing novel cancer prevention strategies.

More Related Videos

Reconstitution Of β-catenin Degradation In Xenopus Egg Extract09:41

Reconstitution Of β-catenin Degradation In Xenopus Egg Extract

Published on: June 17, 2014

Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro07:51

Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro

Published on: March 18, 2019

Related Concept Videos

Catenins01:23

Catenins

Catenins are characterized by multiple binding domains and dynamic structures that allow them to function as linker proteins in cell junction complexes. All catenins, except α-catenin, contain a characteristic protein sequence called the armadillo repeat and are therefore also called armadillo proteins.
Catenins in Cell Junctions
Catenins bind to cell adhesion molecules such as cadherins and link them to different cytoskeletal proteins depending on the type of cell junction. At the adherens...
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
Cadherins in Tissue Organization01:19

Cadherins in Tissue Organization

The cadherins are a superfamily of cell adhesion molecules comprising over 180 variants, with specific tissues expressing a particular combination of cadherin types. Cadherins generally exhibit homophilic binding; i.e., cadherins on one cell bind to cadherins of the same or closely related type on another cell. Thus, cells of the same type have a specific affinity to bind to each other and sort themselves into clusters to form tissues.
Cell Sorting During Development
Cell sorting plays an...
Canonical Wnt Signaling Pathway02:54

Canonical Wnt Signaling Pathway

The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which results in tumor...