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Published on: June 26, 2018
Anticancer activity of ursolic acid on retinoblastoma cells determined by bioinformatics analysis and validation
Dan Zhou1, Qi Bao1, Songbin Fu2
1Department of Ophthalmology, Suzhou High Tech Zone People's Hospital, Suzhou, China.
Background:
This article aims to explore whether ursolic acid (UA) inhibits the progression of retinoblastoma (Rb) by regulating stearoyl-CoA desaturase (SCD).
Methods:
The Gene Expression Omnibus (GEO) database was used to filter the chip, then the GEO2R software was used to analyze the microarray data (GSE97508, GSE24673, and GSE110811). Gene set enrichment analysis (GSEA) was used to analyze the relationship between the expression level of SCD and the proliferation, migration, invasion, and inflammation in Rb patients. SO-RB50 and Y79 cell proliferation, migration, and invasion were assessed by the CCK-8 assay, the colony formation assay, the Transwell assay, and the wound scratch test. The protein expression levels of SCD were measured by western blot. The mRNA expression levels of IL-8, IL-6, CXCL1, and CCL2 were measured by RT-qPCR. The protein expression levels of IL-8 and IL-6 were measured by ELISA. A xenograft nude mouse model was established to evaluate the effect of UA on tumor growth in male BALB/c mice.
Results:
The expression levels of SCD were related to cell proliferation, migration, invasion, and inflammation. UA inhibited SO-RB50 and Y79 cell proliferation, migration, and invasion. At the same time, UA suppressed tumor growth in the xenograft nude mouse model. Overexpression of SCD promoted SO-RB50 and Y79 cell proliferation, migration, invasion, and inflammation, while SCD knockout inhibited SO-RB50 and Y79 cell proliferation, migration, invasion, and inflammation. Importantly, UA inhibited the proliferation, migration, and invasion of Rb cells through SCD inhibition.
Conclusions:
UA inhibited the proliferation, migration, and invasion of Rb cells through SCD. This provides a new scientific basis for targeted therapy of Rb.
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