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. Author manuscript; available in PMC: 2014 Oct 9.
Published in final edited form as: Clin Cancer Res. 2013 Nov 5;20(2):372–381. doi: 10.1158/1078-0432.CCR-13-1252

FIGURE 3.

FIGURE 3

Transgenic expression of SCCRO5 promotes proliferation and anchorage-independent growth. A, Graph showing results from an MTS assay on NIH-3T3 cells stably expressing SCCRO5 and indicated mutants, which shows increased proliferation in plasmids expressing SCCRO5 but not NLS (SCCRO5_Δ1-10) or PONY (SCCRO5_D195N/A219N/D225N) domain mutants. B, Results from a soft agar assay, which shows increased colony formation in NIH-3T3 cells stably transfected with SCCRO5, compared with that in cells transfected with empty vector and SCCRO5 NLS and PONY domain mutants (bars represent the mean ± SD number of colonies per well of 6-well plates; P < 0.001). C, Western blot analysis, which shows SCCRO5 protein levels and corresponding mRNA levels, on the basis of real-time PCR, in head and neck cancer cell lines. D, Western blot analysis of SCCRO5, with GAPDH as a loading control, on lysates from MDA1386 (low endogenous SCCRO5) and MDA1483 (high endogenous SCCRO5), before and after transfection of two independent shRNA constructs against SCCRO5 or lacZ control, which shows efficient and specific knockdown of SCCRO5. E and F, Graphs from MTS assays showing a more pronounced decrease in the viability of MDA1483 cells, compared with MDA1386 cells, with knockdown of SCCRO5.