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. 2021 Apr 8;40:123. doi: 10.1186/s13046-021-01928-4

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© The Author(s) 2021

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. 4 — Knocking down OXCT1-AS1 markedly suppresses the proliferation of GBM cells in vivo. a OXCT1-AS1 expression levels in GBM cell lines compared with those in the human brain astrocyte cell line NHA. b Three shRNAs targeting OXCT1-AS1 and the empty vector were transfected into A172 and LN229 cells. The inhibitory efficiency was measured by qRT-PCR. c, f After transfecting sh-OXCT1-AS1 and vector, CCK-8 cell proliferation assays were performed at 0, 24, 48, and 72 h. d, e Colony formation assays performed using A172 and LN229 cells transfected with sh-OXCT1-AS1 and the empty vector. g, h Fluorescence microscopy of Ki67 expression after silencing OXCT1-AS1 or transfection with the empty vector. The scale bar represents 100 μm. The bars represent SD (*p < 0.05, **p < 0.01, ***p < 0.001)