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. 2024 Jan 10;56(1):192–209. doi: 10.1038/s12276-023-01147-1

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© The Author(s) 2024

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — a Analysis of IGF1R and EGFR pathway activation in PRKCSH-deficient cells. A549-shCon and A549-shPRK cells or other lung cancer cells, including H292R and H1299 (p53 null) cells transfected with siPRK#2 or siCon, were treated with or without 50 ng/ml TRAIL for the indicated times. The phosphorylation of IGF1R, EGFR, AKT, and ERK1/2 in cell lysates was analyzed by immunoblotting. Representative immunoblots and quantitative analysis of phosphorylated protein levels in each cell line are shown. The quantitative data are shown as the means ± SDs of three independent assays. The statistical significance of differences between two groups was determined with the two-tailed Student’s t test. b The effect of IGF1R overexpression on TNFSF-mediated tumor cell killing in lung cancer cells. A549-shPRK cells were infected with lentivirus containing IGF1R cDNA plasmid, followed by treatment with TRAIL at the indicated concentrations for 24 h. TNFSF-mediated cytotoxicity was analyzed by MTT assay, and activation of caspases was analyzed by immunoblotting. H292R and H1299 (p53 null) cells were transfected with siRNA to IGF1R, followed by treatment with TRAIL at the indicated concentrations for 24 h. TNFSF-mediated cytotoxicity was analyzed by MTT assay, and activation of caspases was analyzed by immunoblotting. c The effect of IGF1R overexpression or knockdown on TNFSF-mediated phosphorylation of AKT and ERK1/2 in lung cancer cells. A549-shPRK cells were infected with lentivirus containing IGF1R cDNA plasmid, or H292R and H1299 (p53 null) cells were transfected with siRNA to IGF1R. Cells were treated with TRAIL for the indicated times, followed by determination of AKT and ERK1/2 phosphorylation by immunoblotting. Representative immunoblots and quantitative analysis of phosphorylated protein levels in each cell line are shown. d The effect of IGF1R overexpression or knockdown on TNFSF-mediated Mcl-1 expression in lung cancer cells. A549-shPRK cells were infected with lentivirus containing IGF1R cDNA plasmid, or H292R and H1299 (p53 null) cells were transfected with siRNA to IGF1R. Cells were treated with TRAIL for the indicated times, followed by determining the expression of Mcl-1L and Mcl-1S by immunoblotting. Representative immunoblots and quantitative analysis of Mcl-1L and Mcl-1S protein levels in each cell line are shown. **p < 0.01, *p < 0.05.