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Chembiochem. 2018 Jul 4;19(13):1359-1364. doi: 10.1002/cbic.201800022. Epub 2018 May 30.

A Forkhead Box Protein C2 Inhibitor: Targeting Epithelial-Mesenchymal Transition and Cancer Metastasis.

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Department of Chemistry and Biochemistry, The University of Texas at Dallas, 800 W. Campbell Road Richardson, Dallas, TX, 75080, USA.
Department of Bioengineering, The University of Texas at Dallas, 800 W. Campbell Road Richardson, Dallas, TX, 75080, USA.
Department of Chemistry and Division of Advanced Material Science, Pohang University of Science and Technology, Pohang, 37673, South Korea.


The epithelial-mesenchymal transition (EMT) has been suggested as a new target for therapeutic intervention of metastatic cancer. Forkhead box protein C2 (FOXC2) is known to be necessary for initiating and maintaining EMT, and therefore bestows on cancer cells metastatic and cancer stem cell (CSC)-like phenotypes, allowing cells to acquire higher motility, invasiveness, self-renewal, and therapy resistance. Here, we describe the first inhibitor of FOXC2, MC-1-F2. MC-1-F2 was able to induce cadherin switching and reverse EMT through the degradation of FOXC2 and blocking of its nuclear localization. In addition, MC-1-F2 was very effective in inhibiting cancer cell migration and invasion. As the first small-molecule inhibitor of FOXC2 and the first compound targeting EMT-associated transcription factor, MC-1-F2 will pave the way for a new anticancer therapeutic agent targeting metastatic cancer and help to elucidate the network of EMT signaling pathways.


cancer metastasis; combinatorial chemistry; drug discovery; epithelial-mesenchymal transition; transcription factor


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