MicroRNA-194 inhibits PRC1 activation of the Wnt/β-catenin signaling pathway to prevent tumorigenesis by elevating self-renewal of non-side population cells and side population cells in esophageal cancer stem cells
Cell and Tissue Research, ISSN: 1432-0878, Vol: 384, Issue: 2, Page: 353-366
2021
- 7Citations
- 2Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations7
- Citation Indexes7
- Captures2
- Readers2
Article Description
Esophageal cancer (EC) is a leading cause of cancer-related deaths worldwide. Recent studies highlight roles for microRNAs (miRNAs) in EC. Microarray analysis identified miR-194 as downregulated in EC. However, little is known about the role of miR-194 in regulating self-renewal or other biological properties of EC stem cells. RT-qPCR and Western blot confirmed the downregulation of miR-194 in EC stem cells and revealed the upregulation of protein regulator of cytokinesis 1 (PRC1) in EC. Dual-luciferase reporter assay confirmed miR-194 targeting of PRC1 resulting in its downregulation. MiR-194 overexpression or PRC1 silencing reduced PRC1 expression, preventing the activation of the Wnt/β-catenin signaling pathway. Inhibition of the Wnt/β-catenin signaling pathway prevented the proliferation, invasion, and self-renewal of EC stem cells while promoting apoptosis. Furthermore, overexpressing miR-194 or silencing PRC1 in nude mice decreased the tumor formation ability of EC stem cells in vivo. Taken together, miR-194 prevents the progression of EC by downregulating PRC1 and inactivating the Wnt/β-catenin signaling pathway.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85100914096&origin=inward; http://dx.doi.org/10.1007/s00441-021-03412-z; http://www.ncbi.nlm.nih.gov/pubmed/33591442; https://link.springer.com/10.1007/s00441-021-03412-z; https://dx.doi.org/10.1007/s00441-021-03412-z; https://link.springer.com/article/10.1007/s00441-021-03412-z
Springer Science and Business Media LLC
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