down-regulation of gep100 causes increase in e-cadherin levels and inhibits pancreatic cancer cell invasiongep100下调导致钙粘蛋白浓度的增加,抑制胰腺癌细胞入侵.pdfVIP
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down-regulation of gep100 causes increase in e-cadherin levels and inhibits pancreatic cancer cell invasiongep100下调导致钙粘蛋白浓度的增加,抑制胰腺癌细胞入侵
Down-Regulation of GEP100 Causes Increase in E-
Cadherin Levels and Inhibits Pancreatic Cancer Cell
Invasion
1 2 1 3 1 1 1
Chuan-gao Xie , Shu-mei Wei *, Jia-min Chen , Xuan-fu Xu , Jian-ting Cai *, Qin-yu Chen , Li-tao Jia
1 Department of Gastroenterology, Second Affiliated Hospital of Zhejiang University College of Medicine, Hangzhou City, Zhejiang Province, China, 2 Department of
Pathology, Second Affiliated Hospital of Zhejiang University College of Medicine, Hangzhou City, Zhejiang Province, China, 3 Department of Gastroenterology, Tenth
Hospital of Tongji University, Shanghai City, China
Abstract
Aims: Invasion and metastasis are major reasons for pancreatic cancer death and identifying signaling molecules that are
specifically used in tumor invasion is of great significance. The purpose of this study was to elucidate the role of GEP100 in
pancreatic cancer cell invasion and metastasis and the corresponding molecular mechanism.
Methods: Stable cell lines with GEP100 knocked-down were established by transfecting GEP100 shRNA vector into
PaTu8988 cells and selected by puromycin. qRT-PCR and Western blot were performed to detect gene expression. Matrigel-
invasion assay was used to detect cancer cell invasion in vitro. Liver metastasis in vivo was determined by splenic injection of
indicated cell lines followed by spleen resection. Immunofluorescence study was used to detect the intracellular localization
of E-cadherin.
Results: We found that the expression level of GEP100 protein was closely related to the invasive ability of a panel of 6
different human pancreatic cancer cell lines. Down-regulation of GEP100 in PaTu8988 cells significantly decreased invasive
activity
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