AI Article Synopsis
- Epigenetic changes in head and neck cancer highlight important factors in its development, particularly the role of the RUNX2 transcription factor, which is linked to worse patient outcomes and increased metastasis.
- Altering RUNX2 levels directly affects the metastatic properties of head and neck squamous cell carcinoma (HNSCC), with additional insights pointing to the involvement of activin A in these processes.
- A key finding is the downregulation of miR-376c-3p, which negatively affects RUNX2 expression and promotes metastasis, suggesting that restoring miR-376c could be a potential therapeutic strategy in managing HNSCC.
Article Abstract
Epigenetic correlates of the head and neck cancer may illuminate its pathogenic roots. Through a gene set enrichment analysis, we found that the oncogenic transcription factor RUNX2 is widely upregulated in the head and neck squamous cell carcinoma (HNSCC) with lymph node metastasis, where it also predicts poor prognosis in patients with HNSCC. Enforced expression of ectopic RUNX2 promoted the metastatic capabilities of HNSCC, whereas RUNX2 silencing inhibited these features. Mechanistic investigations showed that manipulating levels of activin A (INHBA) could rescue or compromise the RUNX2-mediated metastatic capabilities of HNSCC cells. Furthermore, we found that miR-376c-3p encoded within the 3'-untranslated region of RUNX2 played a pivotal role in regulating RUNX2 expression in highly metastatic HNSCC cells, where it was downregulated commonly. Restoring miR-376c expression in this setting suppressed expression of RUNX2/INHBA axis along with metastatic capability. Clinically, we observed an inverse relationship between miR-376c-3p expression and the RUNX2/INHBA axis in HNSCC specimens. In summary, our results defined a novel pathway in which dysregulation of the RUNX2/INHBA axis due to miR-376c downregulation fosters lymph node metastasis in HNSCC. Cancer Res; 76(24); 7140-50. ©2016 AACR.
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| http://dx.doi.org/10.1158/0008-5472.CAN-16-1188 | DOI Listing |
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