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AKT

Tumor Microenvironment Acidity Triggers Lipid Accumulation in Liver Cancer via SCD1 Activation

[Molecular Cancer Research] Investigators found that the acidic tumor microenvironment contributed to lipid accumulation in liver cancer by activating the PI3K/AKT signaling pathway and promoting SCD1-PPARα binding.

Therapeutic Efficacy of FASN Inhibition in Preclinical Models of HCC

[Hepatology] The therapeutic efficacy and the molecular pathways targeted by TVB3664, either alone or with tyrosine kinase inhibitors or the checkpoint inhibitor anti-PD-L1 antibody, were assessed in human HCC cell lines and multiple oncogene-driven HCC mouse models.

Fasting Improves Therapeutic Response in Hepatocellular Carcinoma through p53-Dependent Metabolic Synergism

[Science Advances] Scientists showed in hepatocellular carcinoma (HCC) cells, xenografts, and patient-derived organoids that fasting improved sorafenib efficacy and acted synergistically to sensitize sorafenib-resistant HCC.

Lycium barbarum Polysaccharide Antagonizes Cardiomyocyte Apoptosis by Inhibiting the Upregulation of GRK2 Induced by I/R Injury, and Salvage Mitochondrial Fission/Fusion Imbalance and AKT/eNOS Signaling

[Cellular Signalling] Scientists found that Lycium barbarum polysaccharide limited myocardial infarct size, improved adverse remodeling, and reduced cell death and oxidative stress.

The Inhibition of Panc1 Cancer Cells Invasion by hAMSCs Secretome through Suppression of Tyrosine Phosphorylation of SGK223 (at Y411 Site), C-src (at Y416, Y530...

[Medical Oncology] Researchers employed a co-culture system to clarify the effects of human amniotic mesenchymal stromal cells secretome through tyrosine phosphorylation of c-Src, SGK223, AKT activity, and JAK1/Stat3 signaling in Panc1 pancreatic cancer cells.

BRAF Inhibitors Reprogram Cancer-Associated Fibroblasts to Drive Matrix Remodeling and Therapeutic Escape in Melanoma

[Cancer Research] BRAF inhibitor induced BRAF-CRAF heterodimerization and subsequent activation of ERK signaling in cancer-associated fibroblasts, leading to inactivation of the β-catenin destruction complex.

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