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. 2023 Aug 2;6:805. doi: 10.1038/s42003-023-05166-6

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — a Comparison of proliferation inhibition rate of H1299/H1299R and A549/A549R cells at the indicated concentrations of cisplatin for 72 h. Data represent mean ± SD from three independent experiments. p < 0.001 by Student’s t test. b Western blot analysis showed the protein level of Skp2, MLKL, RIP1 and RIP3 in established cisplatin-resistant (H1299R and A549R) cells and parental (H1299 and A549) cells. c–e Silencing of Skp2 enhances the sensitivity of cisplatin-resistant NSCLC cells to cisplatin. The control or Skp2 siRNA was transiently transfected into H1299R and A549R cells for 72 h. Knockdown of Skp2 was confirmed by Western blot analysis (c). The parental (H1299 and A549) and cisplatin-resistant (H1299R and A549R) cells were transiently transfected for 24 h with the control or Skp2 siRNA, trypsinized, and transferred to a 96-well plate without or with cisplatin (20 μM) for 48 h, followed by cell viability assay (d, e). Data represent mean ± SD from three independent experiments. ***, p < 0.001 by 1-way ANOVA test with Dunnett’s multiple comparisons test, significant difference between groups as indicated. f, g The cisplatin-resistant A549R (f) and parental A549 (g) cells were treated without/with cisplatin (20 μM) for 48 h, WCEs were collected and subjected to Co-IP assay and Western blot analysis. h, i Ectopically expressed MLKL following cisplatin treatment and conducted cell viability assays in H1299R and A549R cells. Data represent mean ± SD from three independent experiments. ***p < 0.001 by Student’s t test, significant difference compared with the cisplatin-treated Vector-tansfected group. j, k H1299R and A549R cells treated with the vehicle control, cisplatin (20 μM), the Skp2 inhibitor SZL P1-41 (10 μM), or cisplatin and SZL P1-41 combination for 48 h, followed by cell viability assays. Data represent mean ± SD from three independent experiments. **p < 0.01, ***p < 0.001 by 1-way ANOVA test with Dunnett’s multiple comparisons test, significant difference compared with the cisplatin-treated group or the SZL P1-41-treated group.