Fig. 1

Docetaxel induces invasion of multiple human breast cancer cell lines toward lymphatics in vitro in a VEGFR3-dependent manner. a Schematic of the in vitro tissue engineered model of the tumor-lymphatic interface in the human breast cancer microenvironment. Our model contains mammary stromal fibroblasts and TNBC cells in a collagen I matrix. LECs are seeded along the underside of the insert system through which tumor cells transmigrate from a basal to luminal fashion. Physiologically relevant flow (1 μm/s) is applied via a pressure head of media to yield delivery of docetaxel. Schematic depicts experimental groups. b Fold change in invasion of MDA-MB-231 tumor cells across the porous membrane in our 3D microenvironment system +/− docetaxel treatment (0.1 μM), +/− MAZ51 (1 μM), and/or in the presence or absence of LECs. c Fold change in invasion of HCC38 tumor cells across the porous membrane in our 3D microenvironment system +/− docetaxel treatment (1 μM), +/− MAZ51 (1 μM), and/or in the presence or absence of LECs. d Fold change in invasion of HCC1806 tumor cells across the porous membrane in our 3D microenvironment system +/− docetaxel treatment (0.1 μM), +/− MAZ51 (1 μM), and/or in the presence or absence of LECs. Fold change calculated as compared to no docetaxel/with LEC control. n ≥ 3 biological replicates. *p < 0.05; **p < 0.01