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. 2022 Jan 27;11(1):2031499. doi: 10.1080/2162402X.2022.2031499

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© 2022 The Author(s). Published with license by Taylor & Francis Group, LLC.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 5. — Glioma-intrinsic ARPC1B controlled the recruitment of macrophages. (a) “Macrophage Chemotaxis” term enriched in high ARPC1B group in CGGA GBM cohort. (b-c) The migration ability of THP1-derived macrophages decreased under the CM from ARPC1B-knockdown glioma cells (Student’s t test, n = 3). (d) PCR results of several chemokines in ARPC1B-knockdown glioma cells (Student’s t test, n = 3). (e) The illustration of the regulating networks between glioma cells and TAMs based on ARPC1B. (* means P < .05, ** means P < .01, *** means P < .001, **** means P < .0001).