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. 2024 Mar 25;43:90. doi: 10.1186/s13046-024-03016-9

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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 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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 3 — Identification of GGT1 as a ropivacaine-responding gene in breast cancer cells. A-B RNA-seq data of ropivacaine- or negative control-treated MCF-7 cells. The scatter plot (A) and volcano map (B) showing differentially-expressed genes. C Heatmap representing the top 50 up-regulated and down-regulated genes in MCF-7 cells treated with ropivacaine or negative control. D The intersection among four databases. E RNA levels of GGT1, TSPAN1 and ANO7 in MCF-7 cells treated with ropivacaine or negative control from RNA-seq data. F-G RNA (F) and protein (G) level of GGT1 in MCF-7 and MDA-MB-231 treated with ropivacaine (10 μM) or negative control for 48 h were was determined by qRT-PCR and western blot, respectively. Results are shown are shown as mean ± S.D from at least three independent experiments. *p < 0.05; **p < 0.01; ***p < 0.001 (unpaired two-tailed Student’s t test)