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. 2021 Oct 28;20:15330338211045831. doi: 10.1177/15330338211045831

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© The Author(s) 2021

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 4. — Knockdown of CBX2 inhibited glioma cell proliferation and invasion and glioma stem cell self-renewal via the downregulation of the Akt/PI3K pathway. (A) Knockdown of CBX2 inhibited the levels of p-Akt and p-GSK-3β, reducing the activity of the Akt/PI3K pathway. The use of EGF, which is an Akt/PI3K pathway agonist, increased the levels of p-Akt and p-GSK-3β. (B and C) CCK-8 and colony formation assays showed that EGF rescued the proliferation of glioma cells. (D) Sphere formation assays showed that the cells in the CBX2-shRNA1 + EGF group were more tumorigenic than those in the CBX2-shRNA1 group (P < .05).

Abbreviations: CBX, ChromoBox; CCK-8, cell counting kit-8; EGF, epidermal growth factor.