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. 2020 May 11;11(5):348. doi: 10.1038/s41419-020-2525-x

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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. 6 — a Heat map generated from the RNA-seq analysis, showing differential gene expression profiles between FTSJ1-overexpression cells and control cells, with three repeats. b Principle component analysis (PCA) of differentially expressed genes revealed a clear separation between FTSJ-overexpression cells and control cells. c KEGG pathway analysis revealing that FTSJ1 activated upregulated pathways. d Pathway analysis showing that FTSJ1-induced downregulated genes were enriched in cancer-associated pathways. e Differentially expressed mRNAs regulated by FTSJ1 overexpression were verified using qRT-PCR in PC9 cells transfected with FTSJ1 or NC. f, g Gene set enrichment analysis (GSEA) of FTSJ1-overexpression cells versus control cells showed that genes were enriched in autophagy and apoptosis pathways. h Upregulation of FTSJ1 suppressed DRAM1 expression; knockdown of FTSJ1 promoted DRAM1 expression. i Rescue assay showed that si-DRAM1 substantially enhanced the inhibitiVE effect of FTSJ1 on NSCLC cell growth. *P < 0.05; **P < 0.01.