Background: Overexpression of PTK7 has been found in multiple cancers and has been proposed to serve as a\nprognostic marker for intrahepatic cholangiocarcinoma. Its role in esophageal cancer, however, remains to be\nclarified. We hypothesize that PTK7 positively regulates tumorigenesis of esophageal cancer.\nMethods: We examined PTK7 expression pattern in human esophageal squamous carcinoma by Oncomine\nexpression analysis and by immunohistochemistry (IHC) staining. We knocked down PTK7 in two esophageal\nsquamous cell carcinoma cell lines, TE-5, and TE-9, by siRNA, and evaluated cell proliferation, apoptosis, and\nmigration ofPTK7-defective cells. Expressions of major apoptotic regulators and effectors were also determined by\nquantitative real-time PCR in PTK7-defective cells. We further overexpressed PTK7 in the cell to evaluate its effects\non cell proliferation, apoptosis, and migration.\nResults: Both Oncomine expression and IHC analyses showed that PTK7 is overexpressed in clinical esophageal\nsquamous cell carcinoma tumors. PTK7 siRNA suppressed cell growth and promoted apoptosis of TE-5 and TE-9.\nPTK7-defective cells further displayed reduced cellular migration that was concomitant with upregulation of Ecadherin.\nConversely, overexpression of PTK7 promotes cell proliferation and invasion, while apoptosis of the PTK7-\noverexpressing cells is repressed. Notably, major apoptotic regulators, such as p53 and caspases, are significantly\nupregulated in siPTK7 cells.\nConclusions: PTK7 plays an oncogenic role in tumorigenesis and metastasis of esophageal squamous carcinoma.\nPTK7 achieves its oncogenic function in esophageal squamous cell carcinoma partially through the negative\nregulation of apoptosis.
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