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. 2020 Dec 9;20:589. doi: 10.1186/s12935-020-01649-2

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 5 — FBXL19 acted as an oncogene in glioma. a FBXL19 expression was examined by RT-qPCR in cells transfected with sh-FBXL19#1/2. b, c The proliferation was evaluated via colony formation and EdU assays (scale bar = 100 μm) in cells with the transfection of sh-FBXL19#1/2. d, e Cell apoptosis was assessed in different groups by caspase 3/8/9 activity detection and TUNEL assay (scale bar = 100 μm). f, g The stemness was appraised by sphere formation assay and RT-qPCR analysis of stemness-associated marker expressions in cells with orwithout -FBXL19 inhibition. **P < 0.01