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. 2019 Oct 10;9:14569. doi: 10.1038/s41598-019-51270-1

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© The Author(s) 2019

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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BMP and TGF-β signaling define divergent molecular identities in glioblastoma. (A) H&E and IHC for pSmad1 (BMP) and pSmad2 (TGF-β) in human glioblastoma surgical specimens (n = 9). (B) Single-cell analysis of pSmad1- and pSmad2-positive cells isolated by laser capture microscopy. (C) Unsupervised clustering of single-cell glioblastoma RNA-seq data using the most variable genes. Cell identity was determined using cell markers for pSmad1 and pSmad2-positive glioma cells. (D) Log-normalized gene expression for selected genes is shown for the SMAD1(+) and SMAD2(+) glioma cell populations defined in 1 C. (E) Gene set enrichment analysis for genes upregulated in SMAD1(+) (left) and SMAD2(+) (right) glioma cell populations identified by analysis of single-cell glioblastoma RNA-seq data. (F) Quantification of PCNA-expression in pSmad1- and pSmad2-positive cells in human glioblastoma surgical specimens (n = 4, 15 HPF/specimen; *p < 0.05).