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Related Experiment Video

Updated: Apr 20, 2026

How to Study Basement Membrane Stiffness as a Biophysical Trigger in Prostate Cancer and Other Age-related Pathologies or Metabolic Diseases

How to Study Basement Membrane Stiffness as a Biophysical Trigger in Prostate Cancer and Other Age-related Pathologies or Metabolic Diseases

Published on: September 20, 2016

AGE-modified basement membrane cooperates with Endo180 to promote epithelial cell invasiveness and decrease prostate

Mercedes Rodriguez-Teja¹, Julian H Gronau, Claudia Breit

¹Department of Surgery and Cancer, Imperial College London, UK; Departamento de Genética, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay.

The Journal of Pathology

|November 20, 2014

Summary

This summary is machine-generated.

Age-related changes in prostate tissue stiffness promote cancer invasion. Blocking a specific domain in Endo180 reversed these invasive behaviors, suggesting a new therapeutic target for prostate cancer.

Keywords:

C-type lectin domain advanced glycation endproducts ageing basement membrane cell contractility collagen crosslinking epithelium invasion matrix stiffness prostate cancer

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Last Updated: Apr 20, 2026

How to Study Basement Membrane Stiffness as a Biophysical Trigger in Prostate Cancer and Other Age-related Pathologies or Metabolic Diseases

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A Cancer Cell Spheroid Assay to Assess Invasion in a 3D Setting

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Published on: November 20, 2015

Area of Science:

Biochemistry
Cell Biology
Oncology

Background:

Age-related thickening and stiffening of the prostate basal lamina correlate with increased cancer risk.
Structural alterations in the basal lamina may trigger mechanotransduction pathways in prostate epithelial cells (PECs), promoting invasiveness.

Purpose of the Study:

To investigate if age-associated basal lamina changes induce mechanotransduction pathways in PECs, leading to cancer progression.
To explore the role of Endo180 and its CTLD2 domain in mediating these effects.

Main Methods:

Developed a 3D model of PEC acini with advanced glycation end-product (AGE)-induced basal lamina thickening and stiffening.
Utilized antibody-targeted blockade of Endo180's CTLD2 domain to assess its impact on PEC behavior.
Correlated in vitro findings with studies in Endo180 mutant mice and human prostate cancer data.

Main Results:

AGE-modified basal lamina induced contractility, loss of polarity, disrupted cell junctions, and invasion in PEC acini.
Targeted blockade of CTLD2 reversed these AGE-induced invasive changes.
In vivo and human data showed concordance, with increased Endo180 expression and AGE levels linked to prostate cancer progression.

Conclusions:

AGE-dependent basal lamina modification drives invasive behavior in non-transformed PECs through a mechanism linked to cancer progression.
Targeting CTLD2 within Endo180 presents a potential therapeutic strategy for prostate cancer and other diseases characterized by basal lamina stiffening.