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Figure 3 | Breast Cancer Research

Figure 3

From: Invasive breast cancer induces laminin-332 upregulation and integrin β4 neoexpression in myofibroblasts to confer an anoikis-resistant phenotype during tissue remodeling

Figure 3

The anoikis resistance of fibroblasts is mediated by binding of laminin-332 to integrin α3β1 and/or integrin β4 neoexpression. Viability of wild-type and integrin β4-expressing (A) InFs, (B) CAFs, and (C) NBFs in the absence or presence of stimulation from cancer cells under anoikis conditions. The figures show fibroblast viability in RSM (open square), MCF7 CM (open diamond), and MDA-MB-231 CM (open circle) in the absence of integrin β4 expression, and viability in RSM (black square), MCF7 CM (black diamond), and MDA-MB-231 CM (black circle) in the presence of integrin β4 expression. (D) Direct comparison of fibroblast viabilities. The viability of wild-type and integrin β4-expressing fibroblasts was compared at 72 hours. Black bar, CAFs; gray bar, InFs; white bar, NBFs; gray box, integrin β4-expressing fibroblasts. (E) Inhibition of the interaction between laminin-332 and integrin. InF and InF/β4 cells were treated with isotype (black bar) and blocking antibodies against integrin β1 (dark gray bar), β4 (light gray bar), and laminin-332 (white bar) for 24 hours under anoikis conditions. (F) Increased viability of CAFs in response to treatment with laminin-332. CAF and CAF/β4 cells were treated with purified laminin-332 (diluted to 10 μM with RSM) in poly-HEMA-treated 96-well plates for 24 hours. Black bar, untreated CAFs; white bar, laminin-322-treated CAFs. Results are expressed as mean ± SD. *P < 0.05; **P < 0.03 versus RSM in poly-HEMA-coated wells. Results are averages of three separate experiments.

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