Table 1.
Association between KIF20A expression and the clinicopathological features of 105 with patients NPC.
Fig 1.
Microarray data reveals KIF20A is upregulated in NPC.
(A) Expression of KIF20A in Array Express (GSE12452) NPC and normal tissues (Mann-Whitney test; P < 0.01). (B) Expression of KIF20A in Array Express (GSE53819) NPC and normal tissue data (Mann-Whitney test; P < 0.05). (C) Expression of KIF20A in Array Express (GSE13597) NPC and normal tissue data (Mann-Whitney test; P < 0.01). (D) Expression of KIF20A in TCGA (head and neck) tumor and normal tissue data (Mann-Whitney test; P < 0.001).
Fig 2.
KIF20A is upregulated in NPC cell lines and tissues.
(A) Reverse transcription (RT)-PCR and real-time PCR analysis of KIF20A mRNA expression in NP69 immortalized nasopharyngeal epithelial cells and eight cultured NPC cell lines. GAPDH was used as a loading control. * P ≤ 0.05. (B) Reverse transcription (RT)-PCR and real-time PCR analysis of KIF20A mRNA expression in three normal nasopharyngeal epithelial biopsies and six NPC tumor samples (three matched samples); GAPDH was used as a loading control. * P ≤ 0.05. (C) Western blotting analysis of KIF20A protein expression in NP69 immortalized nasopharyngeal epithelial cells and eight cultured NPC cell lines. GAPDH was used as a loading control. (D) Western blotting analysis of KIF20A protein expression in three normal nasopharyngeal epithelial biopsies and six NPC tumor samples (three matched samples); GAPDH was used as a loading control. Error bars are standard deviation of the mean (SD) calculated from three experiments performed in parallel.
Fig 3.
Expression of KIF20A in different clinical stages of NPC.
A. Representative images of immunohistochemical staining for KIF20A in normal (control sections) nasopharyngeal tissues and different clinical stages of NPC. B. Average fold change in the mean optical density (MOD) of KIF20A in different clinical stages of NPC compared to normal nasopharyngeal tissues.*P < 0.05.
Fig 4.
KIF20A protein expression is associated with overall survival and progression-free survival in NPC.
(A, B) Kaplan–Meier overall survival (A) and progression-free survival (B) curves for all 105 patients with NPC stratified by high KIF20A expression (n = 45) versus low KIF20A expression (n = 60). Kaplan–Meier overall survival (C, E, G) and disease-free survival (D, F, H) curves for the subgroups of patients with T3–T4 NPC (C, D), lymph node-positive NPC (E, F) and stage III–IV NPC (G, H) stratified by high and low expression of KIF20A. P values were calculated using the log-rank test.
Fig 5.
KIF20A protein expression is associated with overall survival and progression-free survival in NPC patients with NPC who received CCRT.
Kaplan–Meier overall survival (A,C) and progression-free survival (B,D) curves for the subgroups of patients with NPC who received CCRT (A,B) and the advanced clinical stage III-IV NPC patients who treated with CCRT subgroup(C, D) stratified by high and low expression of KIF20A. P values were calculated using the log-rank test.
Table 2.
Univariate and Multivariate Cox regression analysis of the association of various clinicopathological features with overall survival and progression-free survival in 105 patients with NPC.
Table 3.
Univariate and Multivariate Cox regression analysis of the association of various clinicopathological features with overall survival and progression-free survival in 84 clinical stage III-IV NPC patients.
Fig 6.
Effects of KIF20A silencing on cancer cell migration and invasion.
(A)The knock-down efficiency of endogenous KIF20A expression on protein levels were determined by western blotting analysis. (B) SUNE1 and HK1 cells were transfected with two individual KIF20A siRNAs or a scrambled control followed by transwell invasion assays. (C) Effect on migration by wound healing assays. Data are presented as the mean ± SD, and chance was ruled out with Student’s t test.