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Updated: Jun 13, 2026

Molecular Profiling of the Invasive Tumor Microenvironment in a 3-Dimensional Model of Colorectal Cancer Cells and Ex vivo Fibroblasts
Published on: April 29, 2014
CLDN-2 Expression Aligns with Invasion-Associated Epithelial Remodeling in Colorectal Cancer.
Adam R Markowski1, Anna J Sadowska2, Konstancja Mantiuk3
1Department of Hypertensiology, Gastroenterology and Internal Medicine, Medical University of Bialystok, 14 Żurawia Street, 15-540 Bialystok, Poland.
Claudin-2 (CLDN-2) expression in colorectal cancer is linked to epithelial remodeling, increased tumor budding, and nodal spread. This suggests CLDN-2 may drive cancer invasion and dissemination.
Area of Science:
- Oncology
- Cell Biology
- Cancer Research
Background:
- Epithelial junction remodeling is key to colorectal cancer (CRC) progression.
- The role of Claudin-2 (CLDN-2) in CRC-associated epithelial changes and dissemination is unclear.
Purpose of the Study:
- To investigate the association between CLDN-2 expression and spatial epithelial remodeling in CRC.
- To determine if CLDN-2 correlates with tumor budding, adhesion changes, and lymph node metastasis.
Main Methods:
- Retrospective analysis of 54 surgically resected CRCs.
- Integrated clinicopathological data, tumor budding counts, and compartment-specific E-cadherin expression.
- Focused on spatial relationships between CLDN-2, adhesion molecules, and invasion markers.
Main Results:
- Higher CLDN-2 expression correlated with node-positive tumors and advanced stages.
- CLDN-2-high tumors showed increased tumor budding and reduced E-cadherin at the invasive front.
- CLDN-2 expression was spatially linked to tumor budding, lymphovascular invasion, and nodal involvement.
Conclusions:
- CLDN-2 expression is associated with spatial epithelial remodeling in CRC, promoting microinvasion.
- CLDN-2 may facilitate an invasion-associated epithelial phenotype linked to tumor budding and nodal spread.
- Further validation in independent cohorts is warranted.
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