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Golgi phosphoprotein-3 promotes invasiveness of gastric cancer cells through the mTOR signalling pathway
Author(s) -
Jun Liu,
Hongquan Wei,
Liqin Lai,
Yuanyuan Wang,
Xiaoyu Han,
Zhen Zhang
Publication year - 2019
Publication title -
clinical and investigative medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.391
H-Index - 47
eISSN - 1488-2353
pISSN - 0147-958X
DOI - 10.25011/cim.v42i2.32815
Subject(s) - golgi apparatus , phosphoprotein , pi3k/akt/mtor pathway , microbiology and biotechnology , chemistry , signalling pathways , signalling , hedgehog signaling pathway , cancer research , biology , signal transduction , phosphorylation , endoplasmic reticulum
Purpose: Golgi phosphoprotein-3 (GOLPH3) is an oncogene that is overexpressed in multiple cancers and is associated with poor prognosis. The aim of this study was to examine the impact of GOLPH3 on the migration and metastasis of gastric cancer cells. Methods: Following the shRNA-mediated knockdown of GOLPH3, we analyzed cytoskeletal reorganization and cell invasion, migration and adhesion, and determined the impact of components of the mammalian target of the rapamycin (mTOR) signalling pathway. Results: The GOLPH3 mRNA and protein expression were significantly lower in both SGC-7901 and MKN-28 cells as compared with poorly-differentiated BGC-823 cells. The GOLPH3 knockdown also significantly reduced cell invasion in all three cell lines through reduced migration as compared with the non-targeting control sequence group. The GOLPH3 knockdown also reduced F-actin in all three cell lines, and decreased cell adhesion in BGC-823 and SGC-7901 cells. Finally, p-mTOR, p70S6K, p-4EBP1 and RhoA protein levels were significantly downregulated in shGOLPH3-1-treated cells. Conclusions: In conclusion, GOLPH3 increased in poorly-differentiated gastric cancer cells, activating the mTOR-70S6K/4EBP1-RhoA signalling pathway to promote the migration and metastasis of gastric cancer cells.

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