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The C. elegans Intestine As a Model for Intercellular Lumen Morphogenesis and In Vivo Polarized Membrane Biogenesis at the Single-cell Level: Labeling by Antibody Staining, RNAi Loss-of-function Analysis and Imaging

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Cell polarity in morphogenesis and metastasis.

Ian G Macara¹, Luke McCaffrey

¹Department of Cell and Developmental Biology, Vanderbilt University, , Nashville, TN 37215, USA.

Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences

|September 25, 2013

Summary

Cancer cells often lose apical-basal polarity during metastasis. However, this study shows polarity proteins can suppress invasion, and maintaining epithelial character is not essential for tumor growth or spread.

Keywords:

epithelial–mesenchymal transition oncogene tumour suppressor

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Area of Science:

Oncology
Cell Biology
Cancer Research

Background:

Most human cancers originate from epithelial cells, which have distinct apical-basal polarity.
Loss of this polarity is often assumed to be crucial for cancer progression and metastasis.
However, many cancers retain epithelial traits, questioning the necessity of polarity loss for tumor spread.

Purpose of the Study:

To investigate the role of cell polarity machinery in tumor growth and metastasis.
To evaluate whether loss of epithelial character is essential for cancer invasion and colonization.

Main Methods:

Review of existing evidence on polarity proteins in cancer.
Analysis of the relationship between epithelial-mesenchymal transition and metastatic potential.

Main Results:

Polarity proteins can act as potent suppressors of cancer cell invasion.
Loss of epithelial characteristics is not a prerequisite for tumor growth and invasion.
Metastatic colonization can occur without a complete loss of apical-basal polarity.

Conclusions:

The cell polarity machinery plays a significant role in regulating cancer progression.
Maintaining epithelial characteristics does not necessarily hinder tumor invasion or metastasis.
Targeting polarity proteins may offer new therapeutic strategies for cancer treatment.