Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2022 Apr 25;3(4):486–504. doi: 10.1038/s43018-022-00353-6

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2022

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/.

PMC Copyright notice

Fig. 4 — a, Oncosphere formation of SUM159-LM1 breast cancer cells cultured with CM from ST1.6R human lung ECs. CM^–, n = 9; CM⁺, n = 9 technical replicates from 3 independent experiments. Scale bar, 250 μm. b, Analysis of oncosphere formation in SUM159-LM1 breast cancer cells stimulated with HEK293-derived CM containing indicated factors of the vascular niche. Control, n = 24; INHBB, n = 12; LAMA1, n = 12; SCGB3A1, n = 12; OPG, n = 12 technical replicates from 4 independent experiments. c, Oncosphere formation in SUM159-LM1 stimulated with either recombinant activin B (ActB, 50 ng ml^–1) or SCGB3A1 (S3A1, 1 μg ml^–1). ActB^–, n = 8; ActB⁺, n = 8; S3A1^–, n = 9; S3A1⁺, n = 9 technical replicates from 4 (ActB) or 3 (S3A1) independent experiments. a–c, P values were determined by ratio-paired, two-tailed t-test from biologically independent experiments. Boxes depict median with upper and lower quartiles and whiskers indicate minimum and maximum values. d,e, Heatmaps of top upregulated genes in response to ActB (d) or S3A1 (e). f, Schematic diagram of GSEA setup to analyze datasets from patients with breast cancer stratified according to expression of ActB or S3A1 signatures (ActB-S or S3A1-S). g,h, Stem cell-associated gene sets enriched in patients with high ActB-S or S3A1-S in breast cancer samples from Metabric (g) or, GSE14018 (h) datasets. Stem cell signatures are indicated as follows: A, Lim_Mammary stem cell up; B, Lee_Neural crest stem cell up; C, Oswald_Hematopoietic stem cell in collagen gel up; D, Yamashita_Liver cancer stem cell up; E, Ivanova_Hematopoiesis stem cell (all from C2 collection in MSigDB). Dataset from triple-negative breast cancer samples in METABRIC discovery (upper and lower quantile, n = 66) and lung metastases of breast cancer in GSE14018 (upper and lower quantile, n = 8) were analyzed. FDR was determined from P values calculated by random permutation test. *FDR < 0.25, **FDR < 0.05. i, Kaplan–Meier analysis of relapse-free survival of ER^– patients with breast cancer stratified according to expression of ActB-S or S3A1-S; n = 347 patients. P values were determined by log-rank test. j, Diagram summarizing the findings on roles of INHBB and SCGB3A1 in breast cancer metastasis.

Source data