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Related Concept Videos

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.
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Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Cell Adhesion Molecules - Types and Functions01:20

Cell Adhesion Molecules - Types and Functions

Cell adhesion molecules (CAMs) are pivotal to multicellularity and the coordinated functioning of tissues and organ systems. They enable physical interactions between cells and provide mechanical strength to tissues. They also function as receptors for signal transmission across the plasma membrane. The CAMs are broadly classified into four families - integrins, cadherins, selectins, and immunoglobulin-like CAMs (IgCAMs).
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Cell Adhesion Molecules - Types and Functions01:20

Cell Adhesion Molecules - Types and Functions

Cell adhesion molecules (CAMs) are pivotal to multicellularity and the coordinated functioning of tissues and organ systems. They enable physical interactions between cells and provide mechanical strength to tissues. They also function as receptors for signal transmission across the plasma membrane. The CAMs are broadly classified into four families - integrins, cadherins, selectins, and immunoglobulin-like CAMs (IgCAMs).
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Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
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Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
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Related Experiment Video

Updated: May 31, 2026

Characterization of Cell Membrane Extensions and Studying Their Roles in Cancer Cell Adhesion Dynamics
08:11

Characterization of Cell Membrane Extensions and Studying Their Roles in Cancer Cell Adhesion Dynamics

Published on: March 26, 2018

A tumor-suppressing function in the epithelial adhesion protein Trask.

D S Spassov1, C H Wong, G Harris

  • 1Department of Medicine, University of California, San Francisco, CA 94143, USA.

Oncogene
|June 28, 2011
PubMed
Summary

Trask (CDCP1) acts as a tumor suppressor by reducing cancer metastasis. Loss of Trask expression or its phosphorylation in tumors correlates with increased metastasis, suggesting its role in cancer progression.

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Area of Science:

  • Molecular biology
  • Cancer research
  • Cell adhesion

Background:

  • Trask (CDCP1) is a transmembrane glycoprotein in epithelial tissues.
  • Its function as an anti-adhesive effector of Src kinases is under investigation.
  • Previous studies suggested Trask overexpression in some cancers, but newer methods provide more accurate data.

Purpose of the Study:

  • To investigate the role of Trask/CDCP1 in tumor progression.
  • To determine if Trask functions as a tumor suppressor.
  • To identify Trask as a potential tumor suppressor in the 3p21.3 genomic region.

Main Methods:

  • Immunohistochemical survey of human cancer specimens and cell lines to assess Trask expression.
  • Establishment of three experimental models: two gain-of-function and one loss-of-function for Trask.
  • Analysis of Trask expression and phosphorylation in relation to tumor metastasis.

Main Results:

  • Trask expression varies in human cancers, with some tumors showing reduced or lost expression compared to normal tissues.
  • Loss of Trask expression and/or phosphorylation was observed in some cancer cell lines.
  • Inducing Trask expression reduced metastasis in MCF-7 and 3T3v-src cells, while Trask knockdown increased metastasis in L3.6pl cells.

Conclusions:

  • Trask/CDCP1 exhibits tumor-suppressive functions by inhibiting cancer metastasis.
  • Altered Trask expression and phosphorylation are linked to tumor progression.
  • Trask is a potential tumor suppressor candidate on the frequently lost 3p21.3 genomic region.