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. 2018 Feb 13;19(4):335–345. doi: 10.1080/15384047.2018.1423913

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© 2018 Samsung Medical Center, Sungkyunkwan University School of Medicine. 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 4. — EN1 contributes to tumorigenicity of quintuple-negative breast cancer (QNBC) cells. (A and B) The effects of EN1 knockdown on cell proliferation (A) and migration (B) were evaluated via a WST-1 and Boyden chamber assay, respectively. (C and D) The effects of ectopic EN1 overexpression on cell proliferation (C) and migration (D) were evaluated via a WST-1 and Boyden chamber assay, respectively. n = 3; Bars, SE; *P < 0.05, **P < 0.01, Student's t-test. (E) The effect of ectopic EN1 overexpression on HCC38 cell phenotype was monitored via confocal microscopy after staining with an anti-FLAG antibody (green), anti-LAMIN antibody (red), and DAPI (blue). (F) The reduction of HDAC8, UPT11L, and ZIC3 downregulation by siRNA-mediated EN1 knockdown was quantified in treated and control HCC38 and HCC1395 cells by qRT-PCR. (G) The inhibition of cell growth at the indicated times after treatment was evaluated via a WST-1 assay in HCC38 cells treated with 1 nM actinomycin D or DMSO (control). The apoptotic potential of treated cells (%) was determined by flow cytometry and Annexin V assay. The cells were stained with propidium iodide and Annexin V antibody, and their DNA content and intensity were analyzed by flow cytometry. Numbers indicate the percentage of apoptotic cells in each quadrant. EN1 mRNA expression was quantified by qRT-PCR, while EN1 mRNA levels were expressed relative to the calculated EN1/HPRT expression ratio.

Figure 4. — EN1 contributes to tumorigenicity of quintuple-negative breast cancer (QNBC) cells. (A and B) The effects of EN1 knockdown on cell proliferation (A) and migration (B) were evaluated via a WST-1 and Boyden chamber assay, respectively. (C and D) The effects of ectopic EN1 overexpression on cell proliferation (C) and migration (D) were evaluated via a WST-1 and Boyden chamber assay, respectively. n = 3; Bars, SE; *P < 0.05, **P < 0.01, Student's t-test. (E) The effect of ectopic EN1 overexpression on HCC38 cell phenotype was monitored via confocal microscopy after staining with an anti-FLAG antibody (green), anti-LAMIN antibody (red), and DAPI (blue). (F) The reduction of HDAC8, UPT11L, and ZIC3 downregulation by siRNA-mediated EN1 knockdown was quantified in treated and control HCC38 and HCC1395 cells by qRT-PCR. (G) The inhibition of cell growth at the indicated times after treatment was evaluated via a WST-1 assay in HCC38 cells treated with 1 nM actinomycin D or DMSO (control). The apoptotic potential of treated cells (%) was determined by flow cytometry and Annexin V assay. The cells were stained with propidium iodide and Annexin V antibody, and their DNA content and intensity were analyzed by flow cytometry. Numbers indicate the percentage of apoptotic cells in each quadrant. EN1 mRNA expression was quantified by qRT-PCR, while EN1 mRNA levels were expressed relative to the calculated EN1/HPRT expression ratio.