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. Author manuscript; available in PMC: 2013 Jun 7.
Published in final edited form as: Oncogene. 2013 Feb 25;32(23):2828–2835. doi: 10.1038/onc.2013.32

Figure 1.

Figure 1

ERBB2 amplicon repression by HDACI. (a) Fold change in ERBB2 transcript level in MCF10A and BT474 as determined by RT-qPCR in cells treated with DMSO, 500 nM TSA, 10 μg/mL CHX or both TSA and CHX for 4 hr. normalized to GAPDH (n = 6). (b) The amount of ERBB2 transcript detected by standard nuclear run-on (NRO) experiments analyzed by RT-qPCR and normalized to POLR2A. Error bars, s.d.; n.s. = not significant; * = P < 0.05; ** = P < 0.01 by two-tailed Student’s t tests. (c) GRO-seq reads at the ERBB2 locus upon DMSO (green) and TSA (red) treatment. Yellow lines represents overlapping signal between both conditions. Positive and negative strand directions are indicated, and the direction of transcription for ERBB2 is indicated with a red arrow in the positive strand direction. (d) ERBB2 GRO-seq RPKM before and after HDACI treatment (500nM TSA or 3 μM SAHA). *** = P < 10−16 log-likelihood ratio test.