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. 2020 Jul 24;11(7):573. doi: 10.1038/s41419-020-02749-7

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© The Author(s) 2020

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. 4 — a Venn diagram revealed the common up/downregulated genes (adjusted P value < 0.05, fold-change = 2) detected using RNA-seq in HCCC9810 and RBE cells treated with anlotinib; 420 genes were shared in the two cell lines (273 genes upregulated, 147 genes downregulated); b KEGG enrichment analysis based on these differentially expressed genes; c gene set enrichment analysis of mRNA expression profiles of the two cell lines revealed that cell cycle and VEGF signaling pathways were significantly altered after anlotinib treatment of ICC cells; d a weighted gene co-expression network analysis algorithm was implemented to construct the gene co-expression network. The module–trait relationships revealed two modules highly correlated with anlotinib treatment phenotype: the black module (correlation: 0.93, P < 0.01) and the red module (correlation: 0.90, P < 0.01). Pathway annotation showed that the genes in these two critical modules were mainly enriched in the VEGF signaling network and PI3K/AKT signaling pathway.