PT  - JOURNAL ARTICLE
AU  - YU KAMATA
AU  - TOMOKI SUMIDA
AU  - YOSUKE KOBAYASHI
AU  - AKIKO ISHIKAWA
AU  - WATARU KUMAMARU
AU  - YOSHIHIDE MORI
TI  - Introduction of <em>ID2</em> Enhances Invasiveness in <em>ID2</em>-null Oral Squamous Cell Carcinoma Cells <em>via</em> the SNAIL Axis
DP  - 2016 Nov 01
TA  - Cancer Genomics - Proteomics
PG  - 493--497
VI  - 13
IP  - 6
4099  - http://cgp.iiarjournals.org/content/13/6/493.short
4100  - http://cgp.iiarjournals.org/content/13/6/493.full
SO  - Cancer Genomics Proteomics2016 Nov 01; 13
AB  - Aim: Inhibitor of DNA-binding (ID) proteins are negative regulators of basic helix-loop-helix transcription factors that generally stimulate cell proliferation and inhibit differentiation. However, the role of ID2 in cancer progression remains ambiguous. Here, we investigated the function of ID2 in ID2-null oral squamous cell carcinoma (OSCC) cells. Materials and Methods: We introduced an ID2 cDNA construct into ID2-null OSCC cells and compared them with empty-vector-transfected cells in terms of cell proliferation, invasion, and activity and expression of matrix metalloproteinase (MMP). Results: ID2 introduction resulted in enhanced malignant phenotypes. The ID2-expressing cells showed increased N-cadherin, vimentin, and E-cadherin expression and epithelial–mesenchymal transition. In addition, cell invasion drastically increased with increased expression and activity of MMP2. Immunoprecipitation revealed a direct interaction between ID2 and zinc finger transcription factor, snail family transcriptional repressor 1 (SNAIL1). Conclusion: ID2 expression triggered a malignant phenotype, especially of invasive properties, through the ID2–SNAIL axis. Thus, ID2 represents a potential therapeutic target for OSCC.