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. Author manuscript; available in PMC: 2015 Jan 1.
Published in final edited form as: Clin Cancer Res. 2013 Oct 16;20(1):56–67. doi: 10.1158/1078-0432.CCR-13-1255

Figure 2. αB-crystallin overexpression in TNBC cells enhances adhesion to brain endothelium, transendothelial migration, and BBB transmigration in vitro.

Figure 2

(A) Immunocytochemistry analysis of confluent primary HBMEC (passage #4–5) monolayers. The tight junction proteins claudin-5, occludin and ZO-1 were expressed at varied levels throughout the monolayer. HBMEC clusters with elevated expression and appropriate localization of these proteins are shown. Negative controls (mouse or rabbit IgG) are also included. Scale bar = 5 μm. (B) Immunoblot of 231-mCherry breast cancer cells stably expressing vector or αB-crystallin. (C) Adhesion of 231-mCherry cells stably expressing vector or αB-crystallin (αB) to HBMECs. Cells were seeded onto confluent HBMECs for 2 h, washed and attached mCherry-positive cells were scored (mean ± SEM, n = 3, **P < 0.01). (D) Transendothelial migration (TEM) of 231-mCherry-Vector or 231-mCherry-αB cells at 24 h (mean ± SEM, n = 3, **P < 0.01). (E) BBB transmigration in vitro. 231-mCherry-Vector or 231-mCherry-αB cells that transmigrated through two cell layers (HBMECs and astrocytes) were scored at 48 h (mean ± SEM, n = 3, *P < 0.05).