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Published on: January 22, 2021
Snail1 expression in human colon cancer DLD-1 cells confers invasive properties without N-cadherin expression
Shoko Tanaka1,2, Wakako Kobayashi1, Misako Haraguchi1
1Department of Biochemistry and Molecular Biology, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1 Sakuragaoka, Kagoshima 890-8544, Japan.
Abstract:
The epithelial-mesenchymal transition (EMT) is a fundamental characteristic of carcinoma cells. EMT is generally associated with a change in cellular morphology from cobblestone to spindle shape, reduced expression of epithelial markers such as E-cadherin, and enhanced expression of mesenchymal markers such as N-cadherin. This EMT-associated reciprocal expression of E-cadherin and N-cadherin has been called the "cadherin switch". Downregulation of E-cadherin enables cells to dissociate from colonies while upregulation of N-cadherin is associated with increased invasiveness. The transcription factor Snail1 induces these changes in various epithelial cell lines, including canine MDCK cells and human A431 cells. In the present study, we introduced a Snail1 expression vector into human DLD-1 cells and isolated stable transfectants. These cells showed changes in morphology, reduced expression of epithelial marker E-cadherin and occludin, and elevated invasion and migration. However, neither expression of N-cadherin protein nor its corresponding mRNA was detected. Therefore, elevated N-cadherin expression is not required for invasiveness of the cells.
Insights
The epithelial-mesenchymal transition (EMT) involves cellular changes and can increase cancer cell invasion. This study found that while Snail1 induces EMT and invasion, elevated N-cadherin is not required for these effects.
Area of Science:
- Cell Biology
- Molecular Biology
- Cancer Research
Background:
- Epithelial-mesenchymal transition (EMT) is crucial in carcinoma progression.
- EMT involves morphological changes, loss of epithelial markers (e.g., E-cadherin), and gain of mesenchymal markers (e.g., N-cadherin), termed the 'cadherin switch'.
- Snail1 is a key transcription factor driving EMT in various cell lines.
Purpose of the Study:
- To investigate the role of Snail1 in inducing EMT and cellular invasiveness in human DLD-1 cells.
- To determine if N-cadherin upregulation is essential for Snail1-induced invasiveness.
Main Methods:
- Stable transfectants of human DLD-1 cells expressing Snail1 were generated.
- Changes in cell morphology, expression of epithelial markers (E-cadherin, occludin), and mesenchymal markers (N-cadherin) were analyzed.
- Cellular invasion and migration assays were performed.
Main Results:
- Snail1 expression induced morphological changes, reduced E-cadherin and occludin levels, and increased invasion and migration.
- Despite induced invasiveness, neither N-cadherin protein nor mRNA was detected in the transfectants.
- This indicates that N-cadherin is not necessary for Snail1-mediated invasion.
Conclusions:
- Snail1 can promote carcinoma cell invasion and migration through mechanisms independent of N-cadherin upregulation.
- The 'cadherin switch' may not be universally required for EMT-driven invasiveness in all cancer contexts.
- These findings refine our understanding of EMT regulation in cancer progression.
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