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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 3. — Glioma-intrinsic ARPC1B promoted the malignant phenotypes of themselves. (a) Dual Immunofluorescence of ARPC1B and GFAP in clinical GBM samples. (b) The ARPC1B expression and EMT status of glioma cells after two ARPC1B-siRNAs’ transfections. (c-d) The migration ability of glioma cells after ARPC1B knockdown by two ARPC1B-siRNAs (Student’s t test, n = 3). (e-f) The invasion ability of glioma cells after ARPC1B knockdown by two ARPC1B-siRNAs (Student’s t test, n = 3). (g) The percent survival of tumor-bearing mice after U87 with ARPC1B knockdown or negative control implanted intracranially (log-rank test, n = 5). (h) HE and IHC staining of tumors in tumor-bearing mice after U87 with ARPC1B knockdown or negative control implanted intracranially. (* means P < .05, ** means P < .01, *** means P < .001, **** means P < .0001).