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. 2017 Jun 9;7:3121. doi: 10.1038/s41598-017-01443-7

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© The Author(s) 2017

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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Cellular uptake and efflux of ¹⁸F-IRS in HCC827, H1975, H358 and H520 cell lines. (A) The cellular uptake of ¹⁸F-IRS in HCC827 was higher than others H1975, H520 and H358 cell lines at all time. (B) Time-dependent efflux of ¹⁸F-IRS in four cell lines (n = 3). Specificity of ¹⁸F-IRS binding with mutated EGFR in HCC827 cells. (C) A dramatic inhibition of cell uptake in HCC827 was observed in the presence of gefitinib (100 µmol/L). (D) Efflux of ¹⁸F-IRS in HCC827 cell line unblocked and blocked by gefitinib. Data are presented as means ± SD.