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Mechanism of OGT-mediated FASN glycosylation regulating JNK/ICAM1 pathway in Liver cancer stem cell metastasis

GSE269783 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2024/11/11 Platform GPL24676
Summary
We performed transcriptome sequencing analysis on LCSCs with different metastatic abilities. KEGG enrichment showed that genes upregulated during LCSC3 metastasis were related to cell membrane pathways. qPCR and flow cytometry confirmed that FASN expression was significantly upregulated during LCSCs metastasis. ICAM1 affects EMT, invadopodia formation, migration and invasion ability of LCSCs. ICAM1 plays a key role in the process of liver metastasis and the development of hepatocellular carcinoma in mice. FASN is also highly expressed during LCSC metastasis. Silencing FASN reduces the expression level of stemness genes, migration and invasion ability, and self-renewal ability of LCSCs. GSEA analysis indicated that transcriptome sequencing results after FASN knockdown were mainly enriched in the EMT process. FASN affects the expression of ICAM1 through the JNK/c-Jun axis in the MAPK pathway, and OGT is involved in the glycosylation process of ICAM1 regulating FASN, thereby affecting the migration ability of LCSCs.
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Also filed as BioProject PRJNA1123685 and SRA study SRP513749. Searching any of these in the dataset finder brings you back here.

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