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. 2024 Jul 1;22:386. doi: 10.1186/s12951-024-02648-5

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© The Author(s) 2024

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 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. 22 — (A) Survival analysis indicated that miR-182 expression increased the survival of animals (rthotopic xenograft with glioma cells and engineered GICs that stably expressed miR-182). (B and C) Tumor burden analysis via weight and bioluminescence imaging. (D) Weight of tumors derived from U87MG xenografts extracted from SCID mice 21 days after intravenous treatment with Co-SNAs or 182-SNAs. (E) Bioluminescence imaging of xenograft tumors derived from GIC-20 (12 day) after intravenous treatment with Co-SNAs or 182-SNAs. (F) Estimation levels of Ki67 and caspase-3 in xenograft samples. (G) Ki67 and caspase-3 IHC in coronal brain sections of GIC-derived xenografts expressing Co-miR or miR-182. (H and I) Kaplan-Meyer survival estimator curves of SCID mice xenografted with glioma tumors (U87MG and GIC-20) and intravenously treated with Co-SNAs or 182-SNAs.

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