Premium
GPX2 silencing relieves epithelial–mesenchymal transition, invasion, and metastasis in pancreatic cancer by downregulating Wnt pathway
Author(s) -
Li Fuzhou,
Dai Lan,
Niu Jixiang
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29391
Subject(s) - biology , cancer research , wnt signaling pathway , epithelial–mesenchymal transition , microbiology and biotechnology , metastasis , cancer , signal transduction , genetics
Glutathione peroxidase 2 (GPX2) participates in many cancers including pancreatic cancer (PC), and overexpression of GPX2 promotes tumor growth. Herein, we identified the role of GPX2 in epithelial–mesenchymal transformation (EMT), invasion, and metastasis in PC. Bioinformatics prediction was applied to select PC‐related genes. The regulatory function of GPX2 in PC was explored by treatment with short hairpin RNA against GPX2 or LiCl (activator of wingless‐type MMTV integration site [Wnt] pathway) in PC cells. GPX2 level in PC tissues, the levels of GPX2, β‐catenin, Vimentin, Snail, epithelial‐cadherin (E‐cadherin), matrix metalloproteinase 2 (MMP2), MMP9, and Wnt2 in cells were determined. Subsequently, cell proliferation, invasion, and metastasis were assayed. Bioinformatics analysis revealed that GPX2 was involved in PC development mediated by the Wnt pathway. GPX2 was highly expressed in PC tissues. GPX2 silencing downregulated levels of β‐catenin, Vimentin, Snail, MMP2, MMP9, and Wnt2 but upregulated levels of E‐cadherin. It was confirmed that GPX2 silencing suppressed PC cell proliferation, metastasis, and invasion. Furthermore, the trend of EMT and invasion and metastasis of PC induced by the LiCl‐activated Wnt pathway was reversed when the GPX2 was silenced. GPX2 silencing could inhibit the Wnt pathway, subsequently suppress PC development.