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. 2022 Oct 17;3(10):1211–1227. doi: 10.1038/s43018-022-00438-2

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© The Author(s) 2022

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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Extended Data Fig. 1 — (a) Representative images (left) and quantification of phosphorylation signals (right) of receptor tyrosine kinases (RTKs) in PARPi-sensitive and PARPi-resistant ovarian cancer cells. Cell lysates were analyzed using the Human Phospho-RTK Array Kit (ARY001B, R&D Systems) following the manufacturer’s instructions. The quantification for p-ALK is included in the main manuscript (Fig. 1B, left panel). Quantified phosphorylation signals derived from n = 2 antibody spots of indicated RTK. (b) Western blot analysis of indicated proteins in PARPi/platinum-sensitive and PARPi/platinum-resistant ovarian cancer cells. Data are representative of two repeats with similar results. (c) Western blot analysis of indicated proteins in PARPi-sensitive triple-negative breast cancer (TNBC) cells (parental) and TNBC cells with acquired resistance to PARPi (#6 and #15) treated with 50 nM PARPi (talazoparib) or 0.5 μM ALK inhibitor (ALKi; ceritinib), either alone or in combination, for 48 hours. TNBC cells with acquired resistance to PARPi were selected after exposing PARPi-sensitive SUM149 cells to the increasing doses of talazoparib. Data are representative of two repeats with similar results. (d) Cell viability of parental PARPi-sensitive TNBC cells or TNBC cells with acquired resistance to PARPi treated with the indicated dose of cisplatin for 96 hours. Data are represented as mean ± SD of N = 3 independent experiments. Parental vs Resistant #6, ***P = 0.0004; Parental vs Resistant #15, ***P = 0.0006; one-way ANOVA analysis. (e) Representative images of clonogenic assay results in PARPi-resistant ovarian and TNBC cells in the presence of the indicated inhibitor for 12 days. The mean percentage of growth inhibition derived from N = 3 independent experiments of clonogenic assay was used to calculate the combination index (CI) value. Synergistic inhibition of cell proliferation is defined as CI < 1. CER, ceritinib; OLA, olaparib; Comb, combination of ceritinib and olaparib.

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