AI Article Synopsis

  • Studies show that extracellular vesicles (EVs) containing specific miRNAs, like miR-224-5p, are potential biomarkers for colorectal cancer (CRC).
  • The study revealed that miR-224-5p is highly expressed in CRC cells while its target gene, SLC4A4, is expressed at low levels, influencing cancer cell behavior significantly.
  • Elevated levels of miR-224-5p in EVs from cancer-associated fibroblasts (CAFs) enhance CRC cell proliferation, migration, and invasion, suggesting a key role in cancer progression and potential therapeutic targets for CRC treatment.

Article Abstract

More and more studies indicated that extracellular vesicles (EVs) carrying miRNAs have been potential biomarkers of various cancers including colorectal cancer (CRC). This study aims to explore the function of miR-224-5p carried by EVs derived from cancer-associated fibroblasts (CAFs) in CRC. Here, we found that miR-224-5p was highly expressed while SLC4A4 was lowly expressed in CRC cells. Moreover, dual-luciferase reporter gene assay testified that miR-224-5p targeted SLC4A4. The expression of miR-224-5p in CAFs-derived EVs was found to be elevated. It was also testified that CAFs-derived EVs could transfer miR-224-5p into CRC cells. miR-224-5p in CAFs-derived EVs facilitated the proliferation, migration, invasion and anti-apoptosis of CRC cells. Overexpressing miR-224-5p increased the proliferative, migratory and invasive abilities of CRC cells and inhibit CRC cell apoptosis, while overexpressing SLC4A4 caused the opposite result. Research in vitro and in vivo further indicated that miR-224-5p promoted CRC cell progression via binding to its downstream target gene SLC4A4. Rescue assay also demonstrated that overexpressing miR-224-5p reversed the inhibitory effect of overexpressed SLC4A4 on cancer cell growth. In addition, in vivo assay identified that high level of miR-224-5p promoted the growth of cancer cells in mice in vivo. In conclusion, we explored the effect of miR-224-5p in CRC, which helps for further exploration of new methods for CRC targeted therapy.

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http://dx.doi.org/10.1093/carcin/bgab055DOI Listing

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