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Merck
  • Silencing of GP73 inhibits invasion and metastasis via suppression of epithelial-mesenchymal transition in hepatocellular carcinoma.

Silencing of GP73 inhibits invasion and metastasis via suppression of epithelial-mesenchymal transition in hepatocellular carcinoma.

Oncology reports (2017-01-12)
Ying Yang, Qiang Liu, Hua Zhang, Huarong Zhao, Ruin Mao, Zhipeng Li, Sha Ya, Chunli Jia, Yongxing Bao
초록

Epithelial-mesenchymal transition (EMT) is associated with invasion and metastasis of cancer cells. Golgi protein 73 (GP73) is a serum biomarker for hepatocellular carcinoma (HCC) and our previous study demonstrated that the expression of GP73 correlated with aggressive behavior and EMT molecules in HCC. However, its role in metastatic mechanism of HCC is not clear. The aim of this study was to investigate the effect of GP73 on invasion and migration, and underlying mechanism of GP73 involved in EMT of HCC. The expression of GP73 was downregulated by small interfering RNA (siRNA). The metastatic and invasive abilities were analyzed using scratch assay and Transwell assay. Changes in EMT-related molecules were evaluated by western blot and qRT‑PCR analyses, and epithelial-mesenchymal phenotype changes were also observed. Expression of GP73 was upregulated in the more metastatic HCC cell lines. Knockdown of GP73 by siRNA resulted in a significant decrease in migratory and invasive abilities in both MHCC97H and Bel-7404 cell lines. Importantly, EMT-related markers and morphological phenotypes significantly changed following by the inhibition of GP73. Silencing GP73 contributed to the reduction of invasion and metastasis via suppressing EMT in HCC. GP73 may serve as a novel molecular target against EMT in HCC metastasis therapy.

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Sigma-Aldrich
MISSION® esiRNA, targeting human GOLM1