Fig. 2: Identification of ECM1 as pro-angiogenic candidate in D492HER2. | Laboratory Investigation

Fig. 2: Identification of ECM1 as pro-angiogenic candidate in D492HER2.

From: ECM1 secreted by HER2-overexpressing breast cancer cells promotes formation of a vascular niche accelerating cancer cell migration and invasion

Fig. 2

a 77 candidates. Heat map of 77 proteins higher secreted by D492HER2 compared with both D492 and D492M (label-free mass spectrometry secretome data, p < 0.05, threshold fold change greater than or equal to twofold). b Enrichment of angiogenesis-regulating genes in D492HER2 secretome (GO terms). Enrichment of “Regulation of angiogenesis” GO term group GO:0045765 among D492HER2 secretome. Statistical overrepresentation test (Panther DB) was performed using “GO biological process complete” as annotation dataset with Bonferroni correction for multiple testing. c GO:0045765 gene members. Proteins part of GO term group GO:0045765 (Regulation of angiogenesis). d Highest secretion levels of ECM1 and CHI3L1. Secretion levels (label-free quantification LFQ) of the seven candidates from c (left of dotted line) compared WITH secretion levels of commonly known angiogenesis inducers (right of dotted line). e Correlation of ECM1 to eight gene modules. Spearman correlation of ECM1 expression to different gene modules in breast tumor samples (GOBO Genset analysis, Lund University). f DMFS in ECM1+/HER2+ patients. Kaplan–Meier plot of ECM1 in HER2+ tumors showing correlation of high expression with decreased distant metastasis-free survival (DMFS). g ECM1 expression in HER2+ tumors. ECM1 expression in representative HER2+ tumor samples showing low and high expression. Cells were counterstained with hematoxilyn. Scale bar = 100 µm.

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