Original Article
WASF3 is associated with tumour invasiveness and confers a poor prognosis in human gastric cancer
Abstract
Background: WAS protein family member 3 (WASF3) could be activated by extracellular stimuli and affect organization of actin cytoskeleton, then promote cell movement interacting with a complex of proteins. This study was to assess WASF3 expression and its clinical significance in gastric cancer (GC), and its function in GC cell lines.
Methods: WASF3 protein expression was evaluated in 134 GC samples including 62 paired cancer tissues and adjacent normal mucosa by immunohistochemistry (IHC) assay. Their correlation with clinicopathological factors and overall survival after surgery was calculated, and their biological functions in SGC7901 and HGC27 cells in vitro were studied by knock-down of WASF3 using small guide RNA (sgRNA)-directed CRISPR/Cas9 technology.
Results: IHC results displayed that the rate of WASF3 protein high expression was higher in GC tissues than that in normal mucosa (P<0.001). WASF3 high expression was more frequently detected in patients with poor differentiation and distant metastasis (P=0.038 and 0.032, respectively). WASF3 high expression patients had a poorer prognosis upon univariate analysis (P=0.044). Knockdown of WASF3 by CRISPR/Cas9 method demonstrated that migration and invasion of GC cell were significantly decreased, but not affect cell proliferation in vitro.
Conclusions: Our findings indicated that WASF3 over-expression might participate GC progression, and could be an interrupting target in GC metastasis.
Methods: WASF3 protein expression was evaluated in 134 GC samples including 62 paired cancer tissues and adjacent normal mucosa by immunohistochemistry (IHC) assay. Their correlation with clinicopathological factors and overall survival after surgery was calculated, and their biological functions in SGC7901 and HGC27 cells in vitro were studied by knock-down of WASF3 using small guide RNA (sgRNA)-directed CRISPR/Cas9 technology.
Results: IHC results displayed that the rate of WASF3 protein high expression was higher in GC tissues than that in normal mucosa (P<0.001). WASF3 high expression was more frequently detected in patients with poor differentiation and distant metastasis (P=0.038 and 0.032, respectively). WASF3 high expression patients had a poorer prognosis upon univariate analysis (P=0.044). Knockdown of WASF3 by CRISPR/Cas9 method demonstrated that migration and invasion of GC cell were significantly decreased, but not affect cell proliferation in vitro.
Conclusions: Our findings indicated that WASF3 over-expression might participate GC progression, and could be an interrupting target in GC metastasis.
