Up-regulation of SPOCK1 induces epithelial-mesenchymal transition and promotes migration and invasion in esophageal squamous cell carcinoma. 
Invasion and metastasis are the major causes of death in patients with esophageal squamous cell carcinoma (ESCC).  Recent studies have confirmed that SPARC/osteonectin, cwcv and kazal-like domains proteoglycan 1 (SPOCK1) plays multiple roles in cancer progression.  This study aims to explore the clinical characteristics of SPOCK1 in ESCC and its roles in the migration and invasion of ESCC cell lines.  In this study, the up-regulation of SPOCK1 expression was frequently detected in primary ESCC tumor tissues compared with those in non-tumor tissues, which was significantly associated with tumor invasion (p = 0.004) and distant metastasis (p = 0.010).  SPOCK1 was expressed at higher level in TE13 cells as compared to the low malignant Eca109 and TE1 cells.  Overexpression of SPOCK1 in Eca109 cells decreased the expressions of epithelial marker E-cadherin and ZO-1, while increased mesenchymal marker Vimentin and N-cadherin levels.  After ectopic expression of SPOCK1, Eca109 cells exhibited a morphological change from an epithelial cobblestone phenotype to an elongated fibroblastic phenotype, concomitant with cytoskeletal rearrangements and increased migration and invasion, suggesting that EMT occurs.  While silencing SPOCK1 in TE13 cells had the opposite effects.  These results suggest that up-regulation of SPOCK1 in ESCC induces EMT, thus promotes migration and invasion in ESCC cells.