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

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.