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. 2021 Jan 12;13(2):259. doi: 10.3390/cancers13020259

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Epigenetic modulation of SPCA2 in TNBC. (A) Schematic showing hypothetical effect of histone deacetylase inhibitors (HDAC) inhibitors on SPCA2 expression. (B) Representative western blot of histone acetylation in MDA-MB-231 and HS578T cells after treatment with vorinostat (2.5 µM) or romidepsin (5 nM) for 24 h. GAPDH was used as a loading control (C,D) Quantitation of Western blots (n = 3) by densitometry. (E,F) Treatment of MDA-MB-231 cells with HDAC inhibitors vorinostat (2.5, 5, 10 µM) and romidepsin (5, 10, 15 nM) for 24 h resulted in significant dose-dependence increase of the SPCA2 transcript, n = 3. (G,H) Treatment of MDA-MB-231 cells with HDAC inhibitors vorinostat (2.5, 5, 10 µM) and romidepsin (5, 10, 15 nM) for 24 h resulted in significant decrease of the SPCA1 transcript, n = 3. Student’s t-test, *** p < 0.001, ** p < 0.01, * p < 0.05.

Epigenetic modulation of SPCA2 in TNBC. (A) Schematic showing hypothetical effect of histone deacetylase inhibitors (HDAC) inhibitors on SPCA2 expression. (B) Representative western blot of histone acetylation in MDA-MB-231 and HS578T cells after treatment with vorinostat (2.5 µM) or romidepsin (5 nM) for 24 h. GAPDH was used as a loading control (C,D) Quantitation of Western blots (n = 3) by densitometry. (E,F) Treatment of MDA-MB-231 cells with HDAC inhibitors vorinostat (2.5, 5, 10 µM) and romidepsin (5, 10, 15 nM) for 24 h resulted in significant dose-dependence increase of the SPCA2 transcript, n = 3. (G,H) Treatment of MDA-MB-231 cells with HDAC inhibitors vorinostat (2.5, 5, 10 µM) and romidepsin (5, 10, 15 nM) for 24 h resulted in significant decrease of the SPCA1 transcript, n = 3. Student’s t-test, *** p < 0.001, ** p < 0.01, * p < 0.05.