Journal
ISCIENCE
Volume 26, Issue 9, Pages -Publisher
CELL PRESS
DOI: 10.1016/j.isci.2023.107686
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A study found that Fn infection significantly increased the levels of exosomal miR-122-5p in the serum of CRC patients, and the downregulation of miR-122-5p enhanced the metastatic abilities of CRC cells. Fn activated the TGF-beta 1/Smads signaling pathway through the regulation of the miR-122-5p/FUT8 axis to promote EMT.
Fusobacterium nucleatum (Fn) infection and microRNAs (miRNAs) are closely associated with colorectal cancer (CRC) development, but the mechanism by which Fn regulates tumor-suppressive miRNAs via exosomes and facilitates CRC metastasis remains unclear. Here, we identified that Fn infection significantly increased exosomal miR-122-5p levels in the serum of CRC patients and CRC cell culture supernatants through two miRNA panels of high-throughput sequencing and RT-qPCR analysis. In Fn-infected patients, the serum exosomal levels of miR-122-5p were negatively associated with their expression levels of tissues. Downregulated miR-122-5p was demonstrated to enhance the migration, invasion, and metastasis abilities of CRC cells in vivo and in vitro. Secretion of miR-122-5p into exosomes is mediated by hnRNPA2B1. Mechanistically, Fn activated the TGF-beta 1/Smads signaling pathway to promote EMT by regulation of the miR-122-5p/FUT8 axis. In conclusion, Fn infection may stimulate CRC cells to excrete exosome-wrapped miR-122-5p, and activate the FUT8/TGF-beta 1/Smads axis to promote metastasis.
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