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Conflicts of Interest: The author has completed the ICMJE uniform disclosure form (available at https://tbcr.amegroups.org/article/view/10.21037/tbcr-23-53/coif). The author has no conflicts of interest to declare.
Figures
Figure 1
GCH1 induces EMT independent of…
Figure 1
GCH1 induces EMT independent of its BH4-synthesizing activity. In addition to its canonical…
Figure 1
GCH1 induces EMT independent of its BH4-synthesizing activity. In addition to its canonical enzymatic role in synthesizing BH4 which promotes cancer in by itself ①, GCH1 has now been shown to bind and stabilize Vimentin, and in doing so promote epithelial-mesenchymal transitioning ②. By understanding these distinct functions of GCH1, it opens novel specific, or combinatorial, therapeutic breast cancer treatment options which can target mechanistic routes 1 or 2, or both. GCH1, GTP cyclohydrolase I; EGFR, epidermal growth factor receptor; EMT, epithelial-mesenchymal transition.
Wang Z, Zhang N, Zhang M, Jiang Y, Ng AS, Bridges E, Zhang W, Zeng X, Luo Q, Liang J, Győrffy B, Hublitz P, Liang Z, Fischer R, Kerr D, Harris AL, Cai S.Wang Z, et al.Cancer Res. 2023 Oct 13;83(20):3400-3413. doi: 10.1158/0008-5472.CAN-22-3471.Cancer Res. 2023.PMID: 37463466
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