BACKGROUND: Special AT rich sequence binding protein 1 (SATB1) plays a crucial 
role in the biology of various types of human cancer. However, the role of SATB1 
in human nasopharyngeal carcinoma (NPC) remains unknown. In the present study, 
we sought to investigate the contribution of aberrant SATB1 expression in the 
progression of NPC and its association with the Epstein Barr virus (EBV)-encoded 
latent membrane protein 1 (LMP-1).
METHODS: Immunohistochemical analysis was performed to detect SATB1 and LMP-1 
protein in clinical samples, and the association of SATB1 protein expression 
with patient clinicopathological characteristics and LMP-1 expression were 
analyzed. SATB1 expression profiles were evaluated in well-differentiated NPC 
cell line CNE1, poorly-differentiated CNE2Z, undifferentiated C666-1 and 
immortalized nasopharyngeal epithelia NP-69 cells using quantitative RT-PCR, 
western blotting and fluorescent staining. After inhibition the SATB1 expression 
by using SATB1 specific small interfering RNA in these cell lines, the change of 
cell proliferation was investigated by western blotting analysis of PCNA 
(proliferating cell nuclear antigen) expression and CCK-8 assay, and the cell 
migration was assessed by Transwell migration assay. Finally, the expressions of 
SATB1 and PCNA were examined in CNE1 cells that forced LMP-1 expression by 
fluorescent staining and RT-PCR.
RESULTS: Immunohistochemical analysis revealed that SATB1 protein expression was 
elevated in NPC tissues compared to benign nasopharyngeal tissues (P = 0.005). 
Moreover, high levels of SATB1 protein expression were positively correlated 
with clinical stage (P = 0.025), the status of lymph node metastasis (N 
classification) (P = 0.018), distant metastasis (M classification) (P = 0.041) 
and LMP-1 expression status (r = 2.35, P < 0.01) in NPC patients. In vitro 
experiments demonstrated that an inverse relationship between SATB1 expression 
and NPC differentiation status, with SATB1 weakly expressed in NP-69 cells and 
CNE1 cells, and significant increasingly expressed in CNE-2Z and C666-1 cells. 
Targeted knockdown of SATB1 expression obviously attenuated the proliferation 
and migration of highly SATB1-expressing CNE2Z and C666-1 cells, but not NP-69 
and CNE1 cells. Interestingly, forced LMP-1 expression in CNE1 cells led to a 
surprisingly increasing SATB1 expression and nuclear location, companying with 
an up-regulated PCNA expression.
CONCLUSIONS: Our results reveal that EBV LMP-1-mediated over-expression of SATB1 
is associated with NPC progression, suggesting SATB1 may represent a promising 
biomarker and therapeutic target for NPC.