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. 2013 Jun 12;2013:946451. doi: 10.1155/2013/946451

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Copyright © 2013 Ching-Wen Chang et al.

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

PMC Copyright notice

Schematic of the possible signaling pathways regulated by YMGKI-1, through which to inhibit the EMT, stemness properties, and tumorigenicity of head and neck cancer initiating cells (HN-CICs). The HER2/PI3K/MAPK/mTOR signaling pathway plays an important role in self-renewal, survival, and malignancy of CICs. YMGKI-1 would directly or indirectly inhibit the HER2/PI3K/MAPK/mTOR pathway. Further, an YMGKI-1 analogue is predicted to be a potential inhibitor of cyclooxygenase-2 (COX-2) and 5-lipoxygenase (5-LOX) which are related to epithelial-mesenchymal transition (EMT) [7]. YMGKI-1 might also prevent cells from undergoing EMT to gain stem cell properties via inhibiting COX-2 or 5-LOX. (—) refers to known pathway; (- - -) refers to unknown relationship; (……) refers to prediction.