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Hypoxia-induced CD147-enriched migrasomes promote sorafenib resistance in HCC by inducing vasculogenic mimicry via PI3K/AKT/TWIST1 signaling

GSE316455 Homo sapiens Expression profiling by high throughput sequencing 4 samples Submitted 2026/01/21 Platform GPL24676
Summary
Conventional anti-angiogenic drugs (AADs) combined with sorafenib have little success in HCC patients, as the formation of hypoxia areas in tumors and vasculogenic mimicry’s (VM's) non-responsiveness to AADs. Migrasomes are recently discovered extracellular vesicles produced during cell migration. In this study, the results show that hypoxia-induced migrasomes induce the formation of VM and promote the sorafenib resistance. Further studies reveal that hypoxia-induced migrasomes can be taken up by HCC cells via macropinocytosis, which activates PI3K/AKT/TWIST1 signaling. Moreover, CD147 on the surface of hypoxia-induced migrasomes is identified as a key protein in regulating the signaling pathway. Overall, our findings uncover a previously unrecognized mechanism mediated by hypoxia-induced migrasomes and the formation of VM and provide a new method for preventing SFR.
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Direct links to NCBI, no account and no request form: the whole study as GSE316455_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 4 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1402944 and SRA study SRP662167. Searching any of these in the dataset finder brings you back here.

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