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. 2021 Mar 10;9(3):e001946. doi: 10.1136/jitc-2020-001946

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© Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution 4.0 Unported (CC BY 4.0) license, which permits others to copy, redistribute, remix, transform and build upon this work for any purpose, provided the original work is properly cited, a link to the licence is given, and indication of whether changes were made. See https://creativecommons.org/licenses/by/4.0/.

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The role of STAT3 signaling in the protumor effect of the interaction between tumor-associated neutrophils (TANs) and tumor-associated macrophages (TAMs) in intrahepatic cholangiocarcinoma (ICC). (A) CCK8 cell proliferation assay showed ICC cell proliferation after treatment with TANs and TAMs, shRNA-STAT3 or the STAT3 inhibitor S3I-201 (200 μM). Data are shown as the mean±SD (n=6 for each group). (B) Matrigel-invasion assay showed ICC cell invasion after treatment with TANs and TAMs, shRNA-STAT3 or the STAT3 inhibitor S3I-201. Data are shown as the mean±SD (n=6 for each group). (C) Colony-formation activity of ICC cells after treatment with TANs and TAMs, shRNA-STAT3 or the STAT3 inhibitor S3I-201, ***p<0.001. Data are shown as the mean±SD (n=6 for each group). (D) Tumor volume and (E) pulmonary metastasis of mouse xenografts composed of ICC cells treated with TANs and TAMs with or without shRNA-STAT3 or the STAT3 inhibitor S3I-201. *P<0.05, **p<0.01, ***p<0.001. Scale bars: 100 μm. Data are shown as the mean±SD (n=4 for each experiment mice group).