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. 2022 Nov 9;13(11):942. doi: 10.1038/s41419-022-05393-5

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© The Author(s) 2022

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. 1 — A The expression levels of HOXA11-AS in normal brain tissue, LGG (WHO II-III), and GBM in TCGA and GTEx databases. B ROC curve shows the difference of HOXA11-AS expression in normal brain tissue and glioma from TCGA and GTEx databases (AUC = 0.784). C The expression levels of HOXA11-AS in 41 glioma samples, including WHO II (n = 17) and WHO III-IV (n = 24). D The expression levels of HOXA11-AS in astrocyte, LN308, TG905, U251, U87, and LN229 cells were verified by RT-qPCR. The effect of HOXA11-AS overexpression or knockdown on proliferation by CCK8 experiment in U87 (E) and LN229 cells (F). Xenograft mouse models were generated by subcutaneous injection of U87 cells into nude mice. Seven days after implanted, mice were treated with si-NC (n = 7), si-HOXA11-AS#1 (n = 7), and si-HOXA11-AS#2 (n = 7). Representative image of dissected tumors (G), tumor growth curve (H) and tumor weight (I), in si-NC, si-HOXA11-AS#1 and si-HOXA11-AS#2 treated xenograft models with U87 cells. **P < 0.01, ***P < 0.001, ****P < 0.0001.