AI Article Synopsis
- - Angiosarcoma (AS) is a rare but aggressive cancer with limited treatment options, highlighting the need for further research into its vulnerabilities.
- - Researchers identified that the microRNA miR-497 suppresses cell viability and reduces tumor formation and migration in AS by targeting genes like CCND2, CDK6, and VAT1.
- - The study suggests that inhibiting VAT1, which is linked to cancer spread, using a natural compound Neocarzilin A can reduce AS cell migration, providing potential new therapeutic insights.
Article Abstract
Angiosarcoma (AS) is a vascular sarcoma that is highly aggressive and metastatic. Due to its rarity, treatment options for patients are limited, therefore more research is needed to identify possible therapeutic vulnerabilities. We previously found that conditional deletion of drives AS development in mice. Given the role of DICER1 in canonical microRNA (miRNA) biogenesis, this suggests that miRNA loss is important in AS development. After testing miRNAs previously suggested to have a tumor-suppressive role in AS, microRNA-497-5p (miR-497) suppressed cell viability most significantly. We also found that miR-497 overexpression led to significantly reduced cell migration and tumor formation. To understand the mechanism of miR-497 in tumor suppression, we identified clinically relevant target genes using a combination of RNA-sequencing data in an AS cell line, expression data from AS patients, and target prediction algorithms. We validated miR-497 direct regulation of CCND2, CDK6, and VAT1. One of these genes, VAT1, is an understudied protein that has been suggested to promote cell migration and metastasis in other cancers. Indeed, we find that pharmacologic inhibition of VAT1 with the natural product Neocarzilin A reduces AS migration. This work provides insight into the mechanisms of miR-497 and its target genes in AS pathogenesis.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10557590 | PMC |
| http://dx.doi.org/10.1101/2023.09.24.559218 | DOI Listing |
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