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. 2021 Jan 28;40:47. doi: 10.1186/s13046-020-01767-9

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© The Author(s) 2021

Open AccessThis 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. 5 — GOLPH3L promotes the expression of SERPINE1, which regulates tumorigenic activities in breast cancer cells. a Heat map of transcriptome alterations after silencing GOLPH3L expression in T47D cells; p-values are indicated. b Bubble diagram of KEGG pathways (left panel) and GO analysis of pathways (right panel) related to transcriptome alteration after the inhibition of GOLPH3L; p-values< 0.05 are indicated. c The mRNA expression of SERPINE1 was decreased by GOLPH3L silencing, and p-values< 0.01 are indicated. d Protein-protein interactions of differentially expressed mRNA of proteins. e The protein levels of SERPINE1 were higher in breast cancer tissue samples than in adjacent normal tissues (top panel), and the protein levels of GOLPH3L were higher in breast cancer cell lines than in normal mammary epithelial cells (bottom panel). f The expression of GOLPH3L was correlated with SERPINE1 expression, and SERPINE1 overexpression reversed the suppression of SERPINE1 caused by GOLPH3L knockdown. g SERPINE1 promoted the proliferation and survival of breast cancer cell lines; n = 3, * p < 0.05, ** p < 0.01