Figure 5
Enzastaurin inhibits MM-cell adhesion to fibronectin as well as VEGF- and IGF-1–triggered MM-cell migration. (A) Enzastaurin decreases MM-cell adhesion to fibronectin. Spontaneous adherence of enzastaurin-treated and untreated MM cells to fibronectin (20 μg/mL) was measured using calcein-AM. The results are representative of 3 independent experiments performed in quadruplicate. (B) Enzastaurin abrogates VEGF- and IGF-1–triggered MM-cell migration. Growth factor–deprived enzastaurin-treated or untreated MM.1S cells were plated on either a fibronectin-coated or noncoated membrane (8 μm pore size) in a Boyden modified chamber and stimulated with VEGF or IGF-1, respectively. Cells in the lower chamber were counted with a Coulter counter ZBII. The results shown are representative of 3 independent experiments.

Enzastaurin inhibits MM-cell adhesion to fibronectin as well as VEGF- and IGF-1–triggered MM-cell migration. (A) Enzastaurin decreases MM-cell adhesion to fibronectin. Spontaneous adherence of enzastaurin-treated and untreated MM cells to fibronectin (20 μg/mL) was measured using calcein-AM. The results are representative of 3 independent experiments performed in quadruplicate. (B) Enzastaurin abrogates VEGF- and IGF-1–triggered MM-cell migration. Growth factor–deprived enzastaurin-treated or untreated MM.1S cells were plated on either a fibronectin-coated or noncoated membrane (8 μm pore size) in a Boyden modified chamber and stimulated with VEGF or IGF-1, respectively. Cells in the lower chamber were counted with a Coulter counter ZBII. The results shown are representative of 3 independent experiments.

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