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HIF

PD-L1 Blockade Liberates Intrinsic Antitumourigenic Properties of Glycolytic Macrophages in Hepatocellular Carcinoma

[Gut] Scientists elucidated the nature, regulation and functional relevance of PD-L1+ host cells in HCC.

PBLD Inhibits Angiogenesis via Impeding VEGF/VEGFR2-Mediated Microenvironmental Cross-Talk between HCC Cells and Endothelial Cells

[Oncogene] Researchers reported that phenazine biosynthesis-like domain-containing protein (PBLD) inhibited hypoxia-induced angiogenesis via ERK/HIF-1a/VEGF axis in HCC cells.

PBLD Inhibits Angiogenesis via Impeding VEGF/VEGFR2-Mediated Microenvironmental Cross-Talk between HCC Cells and Endothelial Cells

[Oncogene] Phenazine biosynthesis-like domain-containing protein (PBLD) exerted an inhibitory effect on angiogenesis not only via blocking the VEGFR2 expression in endothelial cells, but also through downregulating HIF-1a-induced VEGF expression and secretion in hepatocellular carcinoma cells.

Exosomal circSHKBP1 Participates in Tumorigenesis, Metastasis, Stemness, Macrophage Polarization and Infiltration in Non-small Cell Lung Cancer through PKM2 Mediated Glycolysis

[Molecular Therapy Oncolytics] Scientists explored the biological function of circSHKBP1 in NSCLC. CircSHKBP1 was found to be upregulated in NSCLC tissues and cell lines and was enriched in exosomes derived from NSCLC cells.

Long Non-Coding RNA PAARH Promotes Hepatocellular Carcinoma Progression and Angiogenesis via Upregulating HOTTIP and Activating HIF-1α/VEGF Signaling

[Cell Death & Disease] The authors identified a HCC-related lncRNA, CMB9-22P13.1, which was highly expressed and correlated with advanced stage, vascular invasion, and poor survival in HCC.

Loss of miR-31-5p Drives Hematopoietic Stem Cell Malignant Transformation and Restoration Eliminates Leukemia Stem Cells in Mice

[Science Translational Medicine] Researchers demonstrated a mechanism of HSC malignant transformation through altered energy metabolism and provided a potential therapeutic strategy to treat patients with AML.

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