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Hepatocellular carcinoma after glucose-free microvesicle treatment

ABSTRACT: As tumor progression occurs, liver cancer cells are often in a state of nutrient deprivation, particularly lacking glucose. We found that microvesicles secreted by liver cancer cells under glucose-free conditions can promote tumorigenesis and progression. The specific mechanism involves enhancing neutrophil expression of PD-L1 and VEGFA, thereby suppressing T cell cytotoxicity and promoting angiogenesis.This phenotype is abolished after Ezrin knockout in liver cancer cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE282968 | GEO | 2026/04/01

REPOSITORIES: GEO

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RNA sequencing of neutrophils treated with microvesicles derived from glucose-deprived hepatocellular carcinoma cells.

Project description:Microvesicles derived from glucose-deprived liver cancer cells can promote tumor initiation and progression through neutrophils. This phenomenon can be rescued by knocking down Ezrin. Comparative analysis revealed that microvesicles from Ezrin-knockdown (Ezrin KD) liver cancer cells exhibit downregulation of VEGFA and PD-L1, along with upregulation of angiogenesis and T-cell regulatory pathways.

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Apigenin inhibits tumor angiogenesis by suppressing microvesicle biogenesis

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hepatocellular carcinoma after glucose-free microvesicle treatment

Project description:hepatocellular carcinoma after glucose-free microvesicle treatment

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RNAi profiling by array of SW840 cells after Ezrin knockdown

Project description:Analysis of SW480 cells following knockdown of Ezrin using RNAi. Ezrin is a protein that regulate the organization of cytoskeleton. Ezrin KD SW480 was used to study the role of ezrin in colon cancer. Experiment Overall Design: Knockdown ezrin in SW480 cells and investigate the affection on cell migration and the downstream genes.

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Project description:Ezrin (EZR), a cell membrane to cytoskeleton linker protein, plays key roles in maintaining cellular homeostasis. Its deregulation at various levels strongly correlates with cancer progression, metastasis and higher patient mortality. However, the precise mechanistic basis for its role remains unknown. Recently, we demonstrated that Ezrin participates in EGFR/AKT signaling pathways. Importantly, transitions between active (phosphorylated open) and inactive (dephosphorylated closed) forms of Ezrin is crucial for its function in cancer. Gene expression analysis suggested dysregulation of genes that are functionally linked to cell energetic metabolism with potential implications for cell proliferation, survival and apoptosis. Total RNA was extracted from n=4 for each experimantal group: Transcriptomic analysis was performed on HeLa WT and HeLa Ezrin KO cells.

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Ezrin knockdown in SW480

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p-Ezrin (Thr567) regulates Hippo pathway and Yap in liver

Project description:It has been shown that up regulation activity of CD81(TAPA-1, the portal of entry of Hepatitis C virus) by agonistic antibody results in phosphorylation of Ezrin. We have previously shown that in liver, Ezrin phosphorylation occurs via Syk kinase, causing suppression of hippo intensity, therefore increases sequential Yap activity. The opposite occurs when Glypican-3 (GPC3) or E2 protein of HCV bind to CD81. Mice over-expressing GPC3 in hepatocytes have decreased p-Ezrin(Thr567) and Yap, increased Hippo activity and suppressed liver regeneration. The role of Ezrin in these processes has been speculated, but not proven. We now provide dynamic picture of Ezrin regulates Hippo pathway and Yap. Forced expression of plasmids expressing mutant Ezrin (T567D) (which mimics p-Ezrin(Thr567)) suppressed Hippo activity and activated Yap signaling. And this mutant Ezrin drive more cell proliferation to cell division through up regulated Yap activity in vitro and in vivo. CD81 loses expression, while p-Ezrin(Thr567) increases in JM1 and JM2 hepatocellular carcinoma (HCC) cells. Administration with compound NSC668394, a characterized p-Ezrin(Thr567) antagonist, caused significant decrease in HCC cell proliferation. We additionally present evidence that pEzrin(T567) is also controlled by EGFR and MET. Conclusions: Ezrin phosphorylation, mediated by CD81 associated Syk kinase, is directly involved in regulation of Hippo pathway, Yap levels and growth rates of normal and neoplastic hepatocytes. The finding has mechanistic and potentially therapeutic applications in understanding and regulating growth of hepatocytes and HCC and HCV pathogenesis. We used microarrays to detail the global programme of gene expression in GFP positive hepatocytes of FVB mice adminstration with EzrinT567D plasmids

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