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. 2017 Oct 16;7(2):e1382790. doi: 10.1080/2162402X.2017.1382790

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© 2018 The Author(s). Published with license by Taylor & Francis Group, LLC

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.

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Figure 7. — Modulation of H4K16ac status impacts on microglia tumor supporting phenotype. (A and C) Immunoblot analysis of H4K16ac and H3 in BV2 microglia pre-treated with EX527 (SIRT1 activity inhibitor) or SRT1720 (SIRT1 activity activator) cultured for 4 h as monoculture or with C6 glioma cells as segregated coculture. (B and D) Quantification of the migration of C6 glioma cells in Transwells with BV2 microglia pre-treated with EX527 or SRT1720 in the lower compartment; results are presented relative to those of C6 cells exposed to BV2 microglia control (ctrl), set as 1. (E and G) Immunoblot analysis of H4K16ac and H3 as well as SIRT1 (E) and hMOF (G) in BV2 microglia transfected with SIRT1-specific siRNA (siRNA SIRT1) or hMOF-specific siRNA (siRNA hMOF) or control siRNA (siRNA Ctrl) cultured for 4 h as monoculture or with C6 glioma cells as segregated coculture. (F and H) Quantification of the migration of C6 glioma cells in Transwells with BV2 microglia transfected with siRNA SIRT1, siRNA hMOF or siRNA Ctrl in the lower compartment; results are presented relative to those of C6 cells exposed to BV2 microglia transfected with siRNA Ctrl, set as 1. *P < 0.05, **P < 0.01, ***P < 0.001 and ****P < 0.0001 (two-tailed Student's t-test). Data are from three independent experiments (D and G) and six independent experiments (B and F) (mean and s.d.).