Research Papers:

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

Shuang Shi _, Dong Zhong, Yao Xiao, Bing Wang, Wentao Wang, Fu'an Zhang and Haoyang Huang

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Oncotarget. 2017; 8:40922-40934. https://doi.org/10.18632/oncotarget.16733

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Shuang Shi1,2, Dong Zhong1, Yao Xiao2, Bing Wang1,2, Wentao Wang1,2, Fu’an Zhang1 and Haoyang Huang1,2

1Department of Neurosurgery, The 1st Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China

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

Correspondence to:

Dong Zhong, email: [email protected]

Keywords: syndecan-1, glioma, proliferation and invasion, c-Src/ FAK

Received: June 29, 2016    Accepted: March 16, 2017    Published: March 31, 2017


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.

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