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Gene expression of hepatocellular carcinoma tissue in China Medical University Hospital (CMUH) cohort of Taiwanese patients

ABSTRACT: It’s unknown what, how, and why lipid metabolites involve in cancer prognosis. This work implementing multi-omics measurement in hepatocellular carcinoma (HCC) patient cohort to associate tumoral lipidome, transcriptome, and serological metabolome to disease prognosis. Data indicating that dietary related ether-lipids, e.g., PC O- and PE O-, promote cell mobility and poor prognosis through TRPV2-related cytoskeletal rearrangement. In addition, downregulation of Peroxisome Proliferator-Activated Receptorα (PPARα) and consequential lipophagic deficit increase ether-lipids in cancer cells. Unfortunately, pathological coupling of Very Low-Density Lipoprotein Receptor (VLDLR) overexpression in HCC patients, concordantly deteriorates ether-lipid accumulation and facilitate HCC prognosis via VLDL entrance, the diet direct responding lipoprotein. Knocking out hepatic VLDLR reduce HCC burden in human etiology-related spontaneous HCC mouse model, which demonstrated the pathological causality in HCC. At last, administration of VLDL-Mimicking Nanoparticle encapsulating Lenvatinib, or fenofibrate (PPAR αagonist) could effectively diminished tumor anarchy.

ORGANISM(S): Homo sapiens

PROVIDER: GSE242315 | GEO | 2025/08/29

REPOSITORIES: GEO

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	GSE242315_FPKM.tsv.gz	Tabular
	GSE242315_Reads_count.tsv.gz	Tabular

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