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. 2021 Apr 7;12(4):374. doi: 10.1038/s41419-021-03657-0

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© The Author(s) 2021

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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Fig. 5 — A Decrease in invasion capacity following microtubule inhibitor treatment (Colchicine) in PTEN-null PDCs (P090) overexpressing PTEN edge mutants. Data are shown as the means of triplicates of experiments ± s.d. PDCs expressing edge mutants exhibited significantly fewer invasive cellular projections following colchicine treatment (p-value=0.009, <0.001, and <0.001 for H93Y, C124S, and R130Q, one-sided t test). B Decrease in invasion following microtubule inhibitor treatment in PTEN-null PDCs with exogenous edge mutation (P089-R130Q) observed in microfluid assay; morphological changes captured during therapy are presented below, which reflecting less invasive property. C Development of tubulin aggresomes after microtubule inhibitor treatment in U87MG cells overexpressing PTEN edge mutations. D Decreased invasive branches of PDCs with endogenous edge mutation following microtubule inhibitor treatment. Data are shown as the means of four experimental replicates ± s.d. PDCs with endogenous edge mutations exhibited significantly decreased invasion following colchicine treatment than BKM120 (p-value=0.114, 0.029, and 0.029 for BKM120, Col, and Vin, respectively (P087); p-value=0.029, 0.029, and 0.029 for BKM120, Col, and Vin, respectively (P045), two-sided Wilcoxon test). E–G Intracranial xenograft model was established using PTEN-null PDCs with exogenous edge mutants (P090-R130Q); Five xenografts were treated by vehicle, while seven and eight mice were treated by BKM120 and Colchicine, respectively. E Invasive scoring system to evaluate the severity of invasion in vivo. We redefined the original invasion scoring system into binary classification, “non-invasive/mild” versus “moderate/strong”. The extent of tumor cell transmission via corpus callosum is the main criteria to distinguish the severity of invasion. F Reduction in infiltrative extent following microtubule inhibitor treatment in in vivo models. Colchicine-treated group exhibited greater decrease in invasiveness than BKM120-treated group, however, this was not statistically significant (p-value=0.39, Fisher’s exact test). G Orthotopic xenografts treated by microtubule inhibitor (colchicine) exhibited improved survival outcome compared to vehicle-treated xenografts, while BKM120 treatment failed to show statistically significant improvement of prognosis. Survival analysis was performed using a Kaplan–Meier plot and the log-rank test was used to show statistical differences between survival curves. Col, colchicine; Vin, vinorelbine; n.s., non-significant.