AI Article Synopsis
- The miR-17~92 microRNA cluster is found to be upregulated in various human cancers, including colorectal cancer (CRC), and is known to promote tumor growth and blood vessel formation.
- Researchers observed that transgenic mice with increased levels of miR-17~92 in their intestinal epithelial cells had smaller tumors and reduced blood vessel formation in a CRC model compared to regular mice.
- The study revealed that miR-17~92 helps prevent CRC progression by targeting specific genes that promote tumor angiogenesis, highlighting its complex role as both a potential cancer promoter and suppressor depending on the context.
Article Abstract
The miR-17~92 microRNA (miRNA) cluster host gene is upregulated in a broad spectrum of human cancers including colorectal cancer (CRC). Previous studies have shown that miR-17~92 promotes tumorigenesis and cancer angiogenesis in some tumor models. However, its role in the initiation and progression of CRC remains unknown. In this study, we found that transgenic mice overexpressing miR-17~92 specifically in epithelial cells of the small and large intestines exhibited decreased tumor size and tumor angiogenesis in azoxymethane and dextran sulfate sodium salt (AOM-DSS)-induced CRC model as compared to their littermates control. Further study showed that miR-17~92 inhibited the progression of CRC via suppressing tumor angiogenesis through targeting multiple tumor angiogenesis-inducing genes, TGFBR2, HIF1α, and VEGFA in vivo and in vitro. Collectively, we demonstrated that miR-17~92 suppressed tumor progression by inhibiting tumor angiogenesis in a genetically engineered mouse model, indicating the presence of cellular context-dependent pro- and anti-cancer effects of miR-17~92.
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| http://dx.doi.org/10.1016/j.canlet.2016.04.011 | DOI Listing |
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