Table 1.
PFTK1 and Ki-67 expression and clinicopathologic characteristics on 161 gastric specmens.
Fig 1.
PFTK1 and PCNA expression in human gastric cancer by Western blot analysis.
(A) The protein level of PFTK1 was high in eight representative paired samples of gastric cancer tissue (T) compared with nontumorous adjacent tissues (N). GAPDH was used as a loading control. (B) The bar chart showed the ratio of PFTK1 protein to GADPH. Mean±SD of three independent experiments. (*P<0.05 compared with control nontumorous adjacent tissues).
Fig 2.
Representative photos of PFTK1, Ki-67 expressions in 161 gastric cancer tissues by IHC.
(A -H) Paraffinembedded tissue sections were stained with antibodies for PFTK1 and Ki-67 and counterstained with hematoxylin. (A,E) negative staining of PFTK1, Ki-67 in adjacent normal tissues (×200); (B,F) weak staining of PFTK1, Ki-67 in well differentiated gastric cancer tissues; (C,G) moderate staining of PFTK1, Ki-67 in moderate differentiated gastric cancer tissues; (D,H) strong staining of PFTK1, Ki-67 in poor differentiated gastric cancer tissues, amplification (×100, ×400).
Fig 3.
The relation between PFTK1 and clinical characteristics.
(A) Correlation between PFTK1 and Ki-67 expression in gastric cancer tissues.The correlation between PFTK1 and Ki-67 expression was evaluated by Pearson correlation test (r = 0.833, P<0.001). (B) Kaplan–Meier survival analysis of 161 gastric cancer patients based on PFTK1 expression level. According to the PFTK1 percentages, patients were divided into high PFTK1 expressers and low PFTK1 expressers. And the median survival time and hazard ratio was showed. Patients in the high-expression PFTK1 group had a significantly shorter overall survival (P< 0.01).
Table 2.
Contribution of various potential prognostic factors to survival by univariate analysis in 161 gastric specimens.
Table 3.
Contribution of various potential prognostic factors to survival by Cox regression analysis in 161 gastric specimens.
Fig 4.
The expression of PFTK1 in nontransfected and transfected gastric cancer cells by western blot.
(A) The PFTK1 protein level in SGC7901, MGC803, HGC27, GES1 gastric cell lines. (B) SGC7901 cells were transiently transfected with Flag-PFTK1 plasmid as described above for 48 h. Western blot analysis ectopic expression of PFTK1. (C) MGC803 cells were transiently transfected with PFTK1-siRNA#1, 2, 3, 4 for 48 h. Western blot analysis knockdown expression of PFTK1. The bar chart showed the ratio of PFTK1 protein to GADPH. Mean±SD of three independent experiments. (*P< 0.05).
Fig 5.
PFTK1 regulates the migration and invasion ability of gastric cancer cells.
(A) Migration of cells transfected with Ctrl, Flag-PFTK1, PFTK1-siRNA#4was examined by wound-healing assays. The wound of cells was visualized at 0 h, 24 h, and 48 h. (B) Cell migration transfected with Ctrl, Flag-PFTK1, PFTK1-siRNA#4 was examined by trans-well assays. (C) The cell invasive ability transfected with Ctrl, Flag-PFTK1, PFTK1-siRNA#4 was examined with Matrigel cell culture chambers. The left part showed MGC803 cells transfected with Ctrl, Flag-PFTK1. The right part showed MGC803 cells transfected with Ctrl, PFTK1-siRNA#4. Mean±SD of three independent experiments (*P<0.05). These results show overexpression of PFTK1 can enhance cells migration and invasion, while knockdown PFTK1 reduce cells migration and invasion.
Fig 6.
PFTK1 modulates the proliferation ability of gastric cancer cells.
(A) In vitro Cell Counting Kit (CCK)-8 assay was used to examin cells growth by absorbance at 450 nm at the indicated time. (The data are means± SD from three independent experiments. *P < 0.05) (B) Colony formation analysis of MGC803 cells transfected with Ctrl, Flag-PFTK1, PFTK1-siRNA#4. (C) Cell cycle analysis was shown after transfected with Ctrl, Flag-PFTK1, PFTK1-siRNA#4 by flow cytometry. The Flag-PFTK1 cell number was decreased in G0/G1 phase and the corresponding increasing was observed in S phase compare with Ctrl. The PFTK1-siRNA#4 cell number was increased in G0/G1 phase and the corresponding reduction was observed in S phase compare with Ctrl. The left part showed MGC803 cells transfected with Ctrl, Flag-PFTK1. The right part showed MGC803 cells transfected with Ctrl, PFTK1-siRNA#4. These results show overexpression of PFTK1 can increase cells proliferation, while knockdown PFTK1 reduce cells proliferation.
Fig 7.
The effects of PFTK1 on the related signal pathway.
The effects of PFTK1 on the expression of Cyclin E, PCNA, MMP2, Wnt related pathways such as β-catenin, Dvl1, Dvl2, Naked1 by western blot. Increasing PFTK1 expression promted the expression of Cyclin E, PCNA, Dvl2, Naked1, MMP2, but had not changed the expression of β-catenin, Dvl1. While knocking down endogenous PFTK1 expression showed the opposite result.