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. Author manuscript; available in PMC: 2016 Jul 15.
Published in final edited form as: Cancer Res. 2015 May 7;75(14):2937–2948. doi: 10.1158/0008-5472.CAN-14-3121

Fig. 6. NRP2 expression varies in HNSCC and mediates tumor cell responsiveness to SEMA3F.

Fig. 6

A) Western blot for the expression of receptors in normal oral keratinocytes (NOKSI) and panel of HNSCC cell lines. B) Western blot showing expression of inducible SEMA3F and knockdown or reintroduction of NRP2 expression in UMSCC2 and UMSCC17B cells, respectively. Proliferation assay of UMSCC2-rtTA3-SEMA3F (C) or UMSCC17B-rtTA3-SEMA3F (D) after SEMA3F induction. Cells were treated with control siRNA or NRP2 siRNA (C) or empty vector or NRP2 (D). Migration assay of UMSCC2-rtTA3-SEMA3F (E) or UMSCC17B-rtTA3-SEMA3F (F) cells with no stimulation (Vehicle) or towards 20% FBS. Cells were treated with control siRNA or NRP2 siRNA (E) or empty vector or NRP2 (F). Proliferation and migration were reported as a percentage of control. Statistical significance was determined using one-way ANOVA, *p<0.05, **p<0.01, ***p<0.001.