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Oncotarget. 2017 Jun 20;8(25):40922-40934. doi: 10.18632/oncotarget.16733.

Syndecan-1 knockdown inhibits glioma cell proliferation and invasion by deregulating a c-src/FAK-associated signaling pathway.

Author information

1
Department of Neurosurgery, The 1st Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
2
Experimental Research Center, The 1st Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.

Abstract

Recent studies have shown that increased syndecan-1 (SDC1) expression in human glioma is associated with higher tumor grades and poor prognoses, but its oncogenic functions and the underlying molecular mechanisms remain unknown. Here, we examined SDC1 expression in datasets from The Cancer Genome Atlas and the National Center for Biotechnology Information Gene Expression Omnibus. Elevated SDC1 expression in glioma was closely associated with increases in tumor progression and shorter survival. We also examined SDC1 expression and evaluated the effects of stable SDC1 knockdown in glioma cell lines. SDC1 knockdown attenuated proliferation and invasion by glioma cells and markedly decreased PCNA and MMP-9 mRNA and protein expression. In a xenograft model, SDC1 knockdown suppressed the tumorigenic effects of U87 cells in vivo. SDC1 knockdown decreased phosphorylation of the c-src/FAK complex and its downstream signaling molecules, Erk, Akt and p38 MAPK. These results suggest that SDC1 may be a novel therapeutic target in the treatment of glioma.

KEYWORDS:

c-src/ FAK; glioma; proliferation and invasion; syndecan-1

PMID:
28422726
PMCID:
PMC5522338
DOI:
10.18632/oncotarget.16733
[Indexed for MEDLINE]
Free PMC Article

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