期刊
CANCER CELL INTERNATIONAL
卷 19, 期 1, 页码 -出版社
BMC
DOI: 10.1186/s12935-019-1035-3
关键词
Glioblastoma; SWAP-70; CD44s; Migration; Invasion
类别
资金
- National Natural Science Foundation of China [81772658, 81772665, 81670142, 81972345]
- Jiangsu Provincial Key Research and Development Program [BE2017636, BE2017638]
- Natural Science Foundation of Jiangsu Province [BK20180104]
- Foundation of Jiangsu Province Six Talents Peak [2016-WSN-136, 2017-WSN-120]
- Jiangsu Qing Lan Project
Background Switch-associated protein 70 (SWAP-70) is a guanine nucleotide exchange factor that is involved in cytoskeletal rearrangement and regulation of migration and invasion of malignant tumors. However, the mechanism by which SWAP-70 regulates the migration and invasion of glioblastoma (GB) cells has not been fully elucidated. Methods This study used an online database to analyze the relationship between SWAP-70 expression and prognosis in GB patients. The in vitro wound healing assay and transwell invasion assay were used to determine the role of SWAP-70 in GB cell migration and invasion as well as the underlying mechanism. Results We found that patients with high SWAP-70 expression in the GB had a poor prognosis. Downregulation of SWAP-70 inhibited GB cell migration and invasion, whereas SWAP-70 overexpression had an opposite effect. Interestingly, SWAP-70 expression was positively correlated with the expression of the standard form of CD44 (CD44s) in GB tissues. Downregulation of SWAP-70 also reduced CD44s protein expression, whereas SWAP-70 overexpression enhanced CD44s protein expression. However, downregulation of SWAP-70 expression did not affect the mRNA expression of CD44s. Reversal experiments showed that overexpressing CD44s in cell lines with downregulated SWAP-70 partially abolished the inhibitory effects of downregulated SWAP-70 on GB cell migration and invasion. Conclusions These results suggest that SWAP-70 may promote GB cell migration and invasion by regulating the expression of CD44s. SWAP-70 may serve as a new biomarker and a potential therapeutic target for GB.
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