Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 493-498 |
| Number of pages | 6 |
| Journal | Cancer Genomics and Proteomics |
| Volume | 13 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - Nov 1 2016 |
Fingerprint
All Science Journal Classification (ASJC) codes
- Biochemistry
- Molecular Biology
- Genetics
- Cancer Research
Cite this
Introduction of ID2 enhances invasiveness in ID2-null oral squamous cell carcinoma cells via the SNAIL axis. / Kamata, Yu; Sumida, Tomoki; Kobayashi, Yosuke; Ishikawa, Akiko; Wataru, Kumamaru; Mori, Yoshihide.
In: Cancer Genomics and Proteomics, Vol. 13, No. 6, 01.11.2016, p. 493-498.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Introduction of ID2 enhances invasiveness in ID2-null oral squamous cell carcinoma cells via the SNAIL axis
AU - Kamata, Yu
AU - Sumida, Tomoki
AU - Kobayashi, Yosuke
AU - Ishikawa, Akiko
AU - Wataru, Kumamaru
AU - Mori, Yoshihide
PY - 2016/11/1
Y1 - 2016/11/1
N2 - 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.
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.
UR - http://www.scopus.com/inward/record.url?scp=84994351239&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84994351239&partnerID=8YFLogxK
U2 - 10.21873/cgp.20012
DO - 10.21873/cgp.20012
M3 - Article
C2 - 27807072
AN - SCOPUS:84994351239
VL - 13
SP - 493
EP - 498
JO - Cancer Genomics and Proteomics
JF - Cancer Genomics and Proteomics
SN - 1109-6535
IS - 6
ER -