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. Author manuscript; available in PMC: 2020 Dec 15.
Published in final edited form as: Nat Cell Biol. 2020 May 18;22(6):701–715. doi: 10.1038/s41556-020-0514-z

Extended Data Fig. 8. GATA3 and AP1 cooperate to regulate endocrine resistance and tumor growth in vitro and in vivo.

Extended Data Fig. 8

a, b, Representative brightfield pictures of MCF7P cells (a) and T47D cells (b) with indicated manipulations. The control cells display a typical epithelial cell-like morphology and grow in tightly packed clusters. Cells with both GATA3 knockdown and JUN overexpression have become more spread out (a phenotype of more invasive cancer cells) than the control and the cells with individual manipulation. Magnification, ×100. Scale bar, 100 μm. n=2 independent experiments were performed with similar results.

c, d, GSEA analyses of RNA-seq data for 34 different cancer types including breast cancer (BRCA) from TCGA database showing the correlation of GATA3 (c) and JUN (d) expression levels with the enrichment of cancer hallmark gene sets from MSigDb database. We found that high expression level of JUN was positively associated with the enrichment of EMT pathway in breast cancer, however high expression level of GATA3 was negatively correlated with EMT pathway in breast cancer. The circle size indicates significance level; and the color represents the normalized enrichment score (NES). The nominal P values were determined by empirical gene-based permutation test with Benjamini-Hochberg adjustment.