Journal
CANCERS
Volume 14, Issue 14, Pages -Publisher
MDPI
DOI: 10.3390/cancers14143346
Keywords
LPAR1; neuroblastoma; LPA; tumor metastasis; bioinformatics analysis
Categories
Funding
- National Natural Science Foundation of China [82173084, 82002637]
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The tumor metastasis in high-risk neuroblastoma patients is a significant problem that affects patient survival. This study utilized comprehensive bioinformatics analysis to identify LPAR1 as a potential target for the treatment of neuroblastoma. The decreased expression of LPAR1 in neuroblastoma cells and the migration-inhibitory effects of LPA-LPAR1 axis suggest that LPAR1 may be a promising target for future neuroblastoma treatment.
Simple Summary The tumor metastasis in the bone marrow or other organs in high-risk neuroblastoma patients is a serious problem to tackle and strongly impairs the survival of patients. Novel and effective targets for the treatment of neuroblastoma, especially tumor metastasis, need to be explored. Using multiple databases and analysis methods, LPAR1 was screened out through our comprehensive bioinformatics analysis and found to be positively associated with survival of neuroblastoma patients. LPAR1 was proved to be reduced in neuroblastoma cells compared with non-mailgant cells. LPA-LPAR1 axis showed migration-inhibitory effects on neuroblastoma cells, suggesting that LPAR1 may be a potential target for future treatment of neuroblastoma. Neuroblastoma is the most common extracranial solid tumor in children. Tumor metastasis in high-risk NB patients is an essential problem that impairs the survival of patients. In this study, we aimed to use a comprehensive bioinformatics analysis to identify differentially expressed genes between NB and control cells, and to explore novel prognostic markers or treatment targets in tumors. In this way, FN1, PIK3R5, LPAR6 and LPAR1 were screened out via KEGG, GO and PPI network analysis, and we verified the expression and function of LPAR1 experimentally. Our research verified the decreased expression of LPAR1 in NB cells, and the tumor migration inhibitory effects of LPA on NB cells via LPAR1. Moreover, knockdown of LPAR1 promoted NB cell migration and abolished the migration-inhibitory effects mediated by LPA-LPAR1. The tumor-suppressing effects of the LPA-LPAR1 axis suggest that LPAR1 might be a potential target for future treatment of NB.
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