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. 2020 Jun 17;8:486. doi: 10.3389/fcell.2020.00486

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Copyright © 2020 Yeon, Kim, Jung and Jeoung.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Effects of HDACs on the responses to anti-cancer drugs and melanoma growth. (A) HDAC2 binds to cancer/testis antigen CAGE and directly regulates the expression of p53 to confer resistance to various anti-cancer drugs in melanoma cells (upper). (B) In Malme3M Cells, HDAC3 decreases the expression levels of HDAC6, MDR1, and tubulin β3 (upper). In Malme3M^R cells, HDAC6 interacts with tubulin β3 and confers resistance to anti-cancer drugs (lower). HDAC3 negatively regulates angiogenic potential by decreasing the expression levels of PAI-1 and VEGF (lower). (C) HDAC3 forms a negative feedback loop with miR-326 and regulates the response to anti-cancer drugs as well as the tumorigenic and metastatic potential of melanoma cells. HDAC3 forms positive feedback loops with miR-200b, miR-217, and miR-335 in Malme3M cells. These miRNAs negatively regulate the expression of CAGE. CAGE interacts with EGFR and HER2 and confers resistance to anti-cancer drugs.