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Oncogenic role of protein tyrosine kinase 7 in esophageal squamous cell carcinoma
Author(s) -
Shin WonSik,
Kwon Junhye,
Lee Hae Won,
Kang Moon Chul,
Na HyeWon,
Lee SeungTaek,
Park Jong Ho
Publication year - 2013
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.12194
Subject(s) - cancer research , gene knockdown , cell growth , focal adhesion , downregulation and upregulation , protein kinase b , biology , tyrosine kinase , immunohistochemistry , pathology , cell migration , cell , medicine , signal transduction , cell culture , microbiology and biotechnology , biochemistry , genetics , gene
Esophageal squamous cell carcinoma ( ESCC ) is a common subtype of esophageal cancer that is particularly prevalent in E ast A sian countries. Our previous expression profile analysis showed that the gene encoding protein tyrosine kinase 7 ( PTK 7) is upregulated in ESCC tissues. Here, we aimed to validate PTK 7 as a prognostic factor and a candidate target for molecular treatment of ESCC . Both RT ‐ PCR and Western blot analysis of tissues from ESCC patients revealed that PTK 7 was significantly upregulated in tumor tissue samples of ESCC . Immunohistochemical staining of PTK 7 showed that increased expression of PTK 7 was inversely correlated with overall survival ( P  = 0.021). In vitro knockdown of PTK 7 inhibited proliferation, survival, wound healing, and invasion of ESCC cells. In addition, PTK 7 knockdown decreased phosphorylation of A kt, E rk, and focal adhesion kinase (FAK), important determinants of cell proliferation, survival, and migration. Therefore, our findings suggest that PTK 7 has potential as a prognostic marker for ESCC and might also be a candidate for targeted therapy in the treatment of ESCC .

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