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. 2016 Mar 8;7(16):21799–21811. doi: 10.18632/oncotarget.7985

Figure 4. Effect of PRL-3 on lung cancer cell growth, tumorigenesis and patients' survival.

Figure 4

(A) Anchorage-dependent cell growth of PRL-3 transfectants, as measured by colony formation. (B) Effect of PRL-3 expression on anchorage-independent growth, as assessed by soft agar assay. Mixed: mixed cell clones; Single: single cell clones PRL3-18 and PRL3-20); Mock: vector alone. The data are presented as the mean ± S.D. of three experiments. P < 0.05, compared with control cells (Mock). (C) PRL-3 overexpression and reduced tumorigenicity in nude mice. The volumes of tumors derived from control cells (Mock) and PRL-3 expressing cells (PRL3-mixed and PRL3-18) were evaluated at the indicated times. (D) The weights of tumors derived from three groups were measured when the nude mice were sacrificed. The columns are presented as the mean ± S.D. (n = 6 mice per group). *P < 0.05, compared with control cells (Mock). (E) Decreased PRL-3 expression is correlated with poor survival in NSCLC patients. The probability of overall survival is presented according to PRL-3 RNA expression level in 443 lung adenocarcinoma patients in a published microarray dataset. The patients were divided into high-expression and low-expression groups using the 70% percentile for the level of PRL-3 RNA as a cut-off point. The overall survival curves were produced by the Kaplan-Meier method, and a 2-tailed log-rank test was used to test the differences between the survival curves.