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. Author manuscript; available in PMC: 2020 Dec 4.
Published in final edited form as: Cancer Res. 2014 Sep 9;74(21):6139–6149. doi: 10.1158/0008-5472.CAN-14-0803

Figure 1.

Figure 1.

Mutation of the Smad3 linker phosphorylation sites greatly suppresses tumor growth of CA1a cells, but instead promotes experimental lung metastasis. A, schematic representation of phosphorylation sites of Smad3 and its mutants (3SA and EPSM). B, immunoblot analysis for the linker and C-tail phosphorylation with specific antibodies in CA1a cells infected with the recombinant adenovirus expressing Smad3 (Ad-Smad3) or its mutant (Ad-3SA or Ad-EPSM) with or without TGFβ1 for 1 hour. Ad-GFP was used as a control. Similar results were obtained from three separate experiments. C, gross appearances of tumors formed 5 weeks after orthotopic xenografts of the adenovirus-infected CA1a cells (5 × 105) into NOD/SCID mice (16 mice per group). D, tumor growth kinetics in C. Each point represents the mean tumor volume (mm3) ± SD from 16 tumors per group. *, 0.01 < P < 0.05; **, P < 0.01, compared with Ad-Smad3–infected cells. E, lung metastatic nodules of NOD/SCID mice (16 mice per group) at the ninth week after the tail-vein injection of the adenovirus-infected CA1a cells (1 × 106). Scale bar, 1.0 cm. F, number of metastatic nodules per lung. Each bar represents the number of metastatic nodules ± SD from 16 lungs per group. **, P < 0.01, compared with Ad-Smad3–infected cells.