Fig. 7 | Nature Communications

Fig. 7

From: SREBP1 drives Keratin-80-dependent cytoskeletal changes and invasive behavior in endocrine-resistant ERα breast cancer

Fig. 7

KRT80-changes induce transcriptional changes of cytoskeletal genes. a PCA analyses of RNA-seq profiled MCF7 breast cancer cells or MCF7 cells with ectopic expression of KRT80. b Volcano plots of over-expressed or under-expressed genes in MCF7 cells following KRT80 ectopic expression. For a complete list, see Supplementary Data 2. c Functional enrichment for upregulated genes following KRT80 ectopic expression. d Representative confocal microscopy images showing F-actin (magenta), cortactin (CTTN, green) and DAPI (blue) staining of MCF7-control and MCF7-K80 cells. Scale bars represent 25 μm. Graph shows mean fluorescence intensity of cortactin in MCF7-control and MCF7-K80 cells (n = 40, MCF7; n = 4, MCF7-K80 individual cells). e Kaplan-Meier plot of ERα-positive breast cancer patients dichotomized to average high or low expression for genes upregulated in response to KRT80 over-expression (Panel b). Multivariate statistics are shown on the right inside table. f Current model: long-term AI treatment promotes constitutive activation of SREBP1 leading to pro-survival re-activation of estrogen receptor12, and global cytoskeletal re-arrangements. Cytoskeletal re-organization leads to direct biomechanical changes and promotes pro-invasive behavior

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