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. 2019 Dec 19;48(3):1175–1191. doi: 10.1093/nar/gkz1149

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© The Author(s) 2019. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Figure 3. — Knockdown of PTTG3P with CRISPR/dCas9-KRAB decreased cell proliferation, prolonged metaphase to anaphase transition, and sensitized LUAD cell lines to chemotherapy. (A) Specificity and efficiency of PTTG3P RNA knockdown in H1299 and CL1-5 cell lines compared to that of the knockdown of PTTG1 by with sgRNAs, as determined by a real-time qPCR assay. 18S rRNA served as an internal control; mean, n = 3. (B) PTTG3P knockdown in H1299 and CL1-5 cell lines decreased cell proliferation, and the statistics was performed by two-way ANOVA at the final time point. (C) PTTG3P knockdown delayed the progression from the G2/M phase to the G1 phase, especially 8 hours after entering the cell cycle, as indicated by the dashed rectangle for the H1299 cell line. (D) PTTG3P knockdown prolonged the process of metaphase to anaphase transition when compared to that produced by the control sgRNA, as shown by live-cell time-lapse imaging in H1299 and CL1-5 cell lines. White and red arrows represent metaphase and anaphase, respectively, as defined by Hoechst dye staining. (E) Summary of metaphase to anaphase transition, based on a comparison between the treatment of H1299 and CL1-5 with PTTG3P and control sgRNAs, and the statistics was performed by One-way ANOVA with the multiple comparison test. (F) Viability assays of PTTG3P and control sgRNA-transfected H1299 cells treated with the LUAD clinical drugs paclitaxel and cisplatin; mean, n = 3; *P< 0.05, **P< 0.005, ***P< 0.0005.

Inline graphic — Knockdown of PTTG3P with CRISPR/dCas9-KRAB decreased cell proliferation, prolonged metaphase to anaphase transition, and sensitized LUAD cell lines to chemotherapy. (A) Specificity and efficiency of PTTG3P RNA knockdown in H1299 and CL1-5 cell lines compared to that of the knockdown of PTTG1 by with sgRNAs, as determined by a real-time qPCR assay. 18S rRNA served as an internal control; mean, n = 3. (B) PTTG3P knockdown in H1299 and CL1-5 cell lines decreased cell proliferation, and the statistics was performed by two-way ANOVA at the final time point. (C) PTTG3P knockdown delayed the progression from the G2/M phase to the G1 phase, especially 8 hours after entering the cell cycle, as indicated by the dashed rectangle for the H1299 cell line. (D) PTTG3P knockdown prolonged the process of metaphase to anaphase transition when compared to that produced by the control sgRNA, as shown by live-cell time-lapse imaging in H1299 and CL1-5 cell lines. White and red arrows represent metaphase and anaphase, respectively, as defined by Hoechst dye staining. (E) Summary of metaphase to anaphase transition, based on a comparison between the treatment of H1299 and CL1-5 with PTTG3P and control sgRNAs, and the statistics was performed by One-way ANOVA with the multiple comparison test. (F) Viability assays of PTTG3P and control sgRNA-transfected H1299 cells treated with the LUAD clinical drugs paclitaxel and cisplatin; mean, n = 3; *P< 0.05, **P< 0.005, ***P< 0.0005.