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. Author manuscript; available in PMC: 2018 Dec 28.
Published in final edited form as: Sci Transl Med. 2014 Jun 25;6(242):242ra84. doi: 10.1126/scitranslmed.3008455

Figure 2. Forced COX-2 expression promotes angiogenesis and tumorigenesis.

Figure 2.

(A) CT26 Clone 3 and Clone 4 tumor growth rates were compared with their corresponding COX-2 stable transfectants (Clone 3/COX-2 and Clone 4/COX-2). The tumorigenic proficiencies of the COX-2-transfected cell lines were reversed by treatment with Celecoxib (Cel).

(B) Serum PGE2 concentrations in vivo were measured in mice bearing subcutaneous tumors from CT26 Clone 3 (C3) and Clone 4 (C4) and corresponding COX-2 transfected cell lines. The impact of Celecoxib (Cel) treatment was also assessed. *p=0.007, **p<0.0001 vs. parent group, ANOVA.

(C) The amount of tumor VEGF in vivo as determined by ELISA. N.S.: Non-significant.)

(D) Tumor spheroids were implanted into the cornea to evaluate the role of COX-2 in tumor angiogenesis. Right panel: Quantification of corneal angiogenesis at day 8 and 11. *p=0.008, **p=0.002 versus parent group, Mann-Whitney.

(E) Flow cytometry was used to quantify the percentage of Gr1+CDllb+ myeloid cells in the spleens of CT26 Clone 3 tumor-bearing mice (n=4).

(F) Flow cytometry was used to quantify the percentage of Gr1+CDllb+ myeloid cells in subcutaneous CT26 Clone 3 tumors (n=4).

Data are presented as mean ± SEM.