Hedgehog signaling activation required for glypican-6-mediated regulation of invasion, migration, and epithelial–mesenchymal transition of gastric cancer cells | Zendy

Chen Zeng | Zendy; Ran Yan | Zendy; Guanghua Yang | Zendy; Sen Xiang | Zendy; Zhao Fuli | Zendy

Open Access

Hedgehog signaling activation required for glypican-6-mediated regulation of invasion, migration, and epithelial–mesenchymal transition of gastric cancer cells

Author(s) -

Chen Zeng,

Ran Yan,

Guanghua Yang,

Sen Xiang,

Zhao Fuli

Publication year - 2020

Publication title -

bioscience reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.938

H-Index - 77

eISSN - 1573-4935

pISSN - 0144-8463

DOI - 10.1042/bsr20193181

Subject(s) - glypican 3 , epithelial–mesenchymal transition , vimentin , gli1 , microbiology and biotechnology , cell migration , small interfering rna , transfection , cancer research , chemistry , cancer cell , gene silencing , cell culture , cell , gene knockdown , biology , hedgehog signaling pathway , cancer , signal transduction , metastasis , immunology , biochemistry , immunohistochemistry , genetics , hepatocellular carcinoma , gene

Gastric cancer (GC) is the fifth most common cancer worldwide and one of the most aggressive cancers in China. Glypican 6 is highly expressed in gastric adenocarcinoma and may act as a diagnostic and prognostic marker; however, the functional importance and molecular mechanism of glypican 6 in GC remains unclear. In the current study, we aimed to reveal the function and mechanism of glypican 6 in two GC cell lines: MKN-45 and SGC-7901. We found higher expression of glypican 6 in MKN-45 and SGC-7901 cells than in cells from the normal gastric mucosa epithelial cell line GES-1. Glypican 6 knockdown suppressed MKN-45 and SGC-7901 cell proliferation. A Transwell assay confirmed that glypican 6 silencing inhibited the migration and invasiveness of MKN-45 and SGC-7901 cells. Epithelial-to-mesenchymal transition (EMT) markers were determined by western blotting, and the results showed reduced Vimentin expression and elevated E-cadherin expression in glypican 6 short interfering RNA (siRNA) transfected MKN-45 and SGC-7901 cells. However, glypican 6 overexpression in GES-1 cells showed no significant promotion on GES-1 cells proliferation and migration. Further studies confirmed that glypican 6 siRNA regulated Hedgehog and Gli1 signaling and participated in the function of glypican 6 on MKN-45 and SGC-7901 cell migration and invasion. Our findings suggest that decreased glypican 6 expression inhibits the migration and invasion ability of GC cells.

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