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. 2020 Jul 31;12(8):2122. doi: 10.3390/cancers12082122

Figure 1.

Figure 1

Diagram of molecular pathways involving CSC during the development of BM-TNBC. CSCs in TNBC bulk tumor must invade through the extracellular matrix in primary bulk tumors, intravasate blood vessels, survive the turbid flow of the blood circulation in vasculature, escape from immune surveillance, arrest in the capillary bed, and extravasate blood brain barrier (BBB), with subsequent tumor growth into brain metastasis involving microenvironmental niche–dormant cell interactions, neuroinflammatory cascades, and neovascularization. EMT: epithelial–mesenchymal transition; CAF: cancer-associated fibroblast; IL: interleukin; ATG: autophagy-related protein; VEGF: vascular endothelial growth factor; Exo-miR: microRNA enriched exosome; STAT: signal transducer and activator of transcription; JAK: janus kinase; uPA: urokinase plasminogen activator; MMP: matrix metalloproteinase; PD-L1: programmed death-1ligand 1; CXCL12: stromal cell-derived factor 1; CXCR4: C-X-C chemokine receptor type 4; Ang2: angiopoietin2; ZO: zonula occludens; SOX: SRY-box transcription factor; OCT4: octamer-binding transcription factor 4; PTEN: phosphatase and tensin homolog; TIMP: metallopeptidase inhibitor; MIF: macrophage migration inhibitory factor; SNAIL: zinc finger protein SNAI1; CCL2: monocyte chemoattractant protein-1; iba1+: ionized calcium binding adaptor myeloid cells.