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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. 7. SEMA3F functions as a tumor and metastasis suppressor in vivo.

Fig. 7

Tumor growth of UMSCC2-rtTA3-SEMA3F (A) and UMSCC17B-rtTA3-SEMA3F (B) after SEMA3F induction via doxy chow. Cervical lymph node metastasis was evaluated as the percentage of metastatic lymph nodes in control and doxy-fed animals for UMSCC2-rtTA3-SEMA3F (C) and UMSCC17B-rtTA3-SEMA3F (D). Microvessel density for lymphatic (LYVE-1) and blood (CD31) vessels was evaluated in the tumor and muscle of tongues for UMSCC2-rtTA3-SEMA3F (E) and UMSCC17B-rtTA3-SEMA3F (F). Microvessel density was reported relative to the average density in vessels/µm. Statistical significance was determined using Student’s t-test, *p<0.05, **p<0.01, ***p<0.001. Immunofluorescent staining of tumors from control and doxy-fed animals for UMSCC2-rtTA3-SEMA3F (G) and UMSCC17B-rtTA3-SEMA3F (H) revealed a higher density and size of vessels in control animals. Lymphovascular invasion by cancer cells is indicated by white arrowheads. I) Proposed mechanism for the role of SEMA3F loss in HNSCC. See text for details.