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hepatic cells

TM4SF5-Dependent Crosstalk between Hepatocytes and Macrophages to Reprogram the Inflammatory Environment

[Cell Reports] Scientists investigated the role of TM4SF5 in communication between hepatocytes and macrophages and its possible influence on the inflammatory microenvironment that may lead to nonalcoholic fatty liver disease.

Liver Sphingomyelin Synthase 1 Deficiency Causes Steatosis, Steatohepatitis, Fibrosis and Tumorigenesis: An Effect of Glucosylceramide Accumulation

[iScience] Investigators implicated that glucosylceramide accumulation was one of triggers promoting the development of nonalcoholic fatty liver disease into non-alcoholic steatohepatitis, then, fibrosis and tumorigenesis.

MET Inhibition Enhances PARP Inhibitor Efficacy in Castration-Resistant Prostate Cancer by Suppressing the ATM/ATR and PI3K/AKT Pathways

[Journal of Cellular and Molecular Medicine] Researchers demonstrated that mesenchymal–epithelial transition (MET) inhibition enhanced sensitivity of CRPC to poly adenosine diphosphate–ribose polymerase (PARP) inhibitors by suppressing the ATM/ATR and phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) pathways.

Genetically Edited Hepatic Cells Expressing the NTCP-S267F Variant are Resistant to Hepatitis B Virus Infection

[Molecular Therapy-Methods & Clinical Development] Investigators introduced NTCP-S267F variant and tested the infectivity by hepatitis B virus in genetically edited hepatic cells.

Inhibition of Extracellular Vesicle-Associated MMP2 Abrogates Intercellular Hepatic miR-122 Transfer to Liver Macrophages and Curtails Inflammation

[iScience] Inhibition of matrix metalloprotease 2 (MMP2) restricted functional transfer of hepatic miRNAs across the hepatic and non-hepatic cell boundaries and by targeting MMP2, scientists could reduce the innate immune response in mammalian liver by preventing intra-tissue miR-122 transfer.

Nanoparticle Delivery of miR-122 Inhibits Colorectal Cancer Liver Metastasis

[Cancer Research] Researchers revealed that delivery of miR-122 was associated with downregulation of key genes in involved in metastatic and cancer inflammation pathways, including several pro-inflammatory factors, matrix metalloproteinases, and other extracellular matrix degradation enzymes.

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