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. 2017 Feb 7;114(8):E1413–E1421. doi: 10.1073/pnas.1621161114

Fig. 1.

Fig. 1.

Loss of RhoA in human fibroblasts reduces their tumor-inhibitory capacity in vitro and induces their tumor-stimulatory capacity in vivo. (A) qRT-PCR for RhoA expression in BjhTERT, BjhTERT–cont-cas9, and BjhTERT RhoA-KO fibroblasts. The y axis indicates the values of expression level of RhoA gene normalized to the TBP reference gene. The x axis shows the cDNA samples. Data are means with 0.95 confidence intervals. ***P = 0.00029 (one-way ANOVA with three levels). (B) Representative Western blots of BjhTERT, BjhTERT–cont-cas9 and BjhTERT RhoA-KO fibroblasts, for RhoA protein levels in total cell lysate (as indicated). Actin protein levels are shown as loading control. (C) Inhibitory capacity of BjhTERT–cont-cas9 and BjhTERT RhoA-KO fibroblasts as confluent monolayers (4-d-old) tested in coculture with PC3 mRFP prostate cancer cells. Data are proliferation ratios of PC3 mRFP cells after 6 d coculture with fibroblasts. ***P < 10−10. (D) Tumor volumes in SCID mice injected with mixtures of PC3 mRFP cells with BjhTERT–cont-cas9 fibroblasts or BjhTERT RhoA-KO fibroblasts (as indicated). PC3 mRFP alone and with BjhTERT fibroblasts did not form tumors (not shown for clarity). Data are means of three independent experiments. ***P < 10−10. See details and statistical analysis in Fig. S3.