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The adhesin RadD enhances Fusobacterium nucleatum tumor colonization and colorectal carcinogenesis

GSE245617 Homo sapiens Expression profiling by high throughput sequencing 9 samples Submitted 2024/06/11 Platform GPL24676
Summary
Fusobacterium nucleatum can bind to host cells and potentiate intestinal tumorigenesis. Here, we used a genome-wide screen to identify an adhesin, RadD, which facilitates the attachment of F. nucleatum to CRC cells in vitro. RadD directly binds to CD147, a receptor overexpressed on CRC cell surfaces, which initiated a PI3K-AKT-NF-κB-MMP9 cascade, subsequently enhancing tumorigenesis in mice. Clinical specimen analysis showed that elevated radD gene levels in CRC tissues correlated positively with activated oncogenic signaling and poor patient outcomes. Finally, blockade of the interaction between RadD and CD147 in mice effectively impaired F. nucleatum attachment and attenuated F. nucleatum-induced oncogenic response. Together, our study provides insights into an oncogenic mechanism driven by F. nucleatum RadD and suggests that the RadD-CD147 interaction could be a potential therapeutic target for CRC.
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Direct links to NCBI, no account and no request form: the whole study as GSE245617_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 9 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1029163 and SRA study SRP466881. Searching any of these in the dataset finder brings you back here.

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