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. 2019 Apr 15;19:354. doi: 10.1186/s12885-019-5562-z

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 2 — Targeting PCAT-1 inhibits c-Myc. a: Relative mRNA expression of c-Myc analysed by qRT-PCR in JHU029 and Cal27 cells with or without transfection of siRNA to PCAT1. Control siRNA was used in parallel. GAPDH gene was used as internal control. b: Cell lysates from JHU029 and Cal27 cells with control or siRNA to PCAT-1 were subjected to Western blot analysis for the c-Myc using specific antibody. The membrane was reprobed with antibody to GAPDH as an internal control. Right panel is quantitative representation of Western blot band intensities using Image-J software. c: Relative mRNA expression of c-Myc in HNSCC tumors (n = 14) compared to the adjacent non-tumor tissues analysed by qRT-PCR. 18 s gene used as internal control. d: Correlation analysis of PCAT-1 and c-Myc expression in HNSCC tumor samples (n = 14). The relationship was evaluated by Pearson’s correlation coefficient (linear regression) with 95% confidence. e: In-silico correlation analysis of expression between PCAT-1 and c-Myc in the HNSCC patient samples of TCGA data analysed by GEPIA (http://gepia.cancer-pku.cn). Small bar indicates standard error (*, p < 0.05; ** p < 0.01; ***p < 0.001)