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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Angiogenesis Inhibitors, Antineoplastic Agents, Carcinoma, Hepatocellular, Cell Line, Tumor, Cell Movement, Cell Survival, Curcumin, Humans, Liver Neoplasms, Matrix Metalloproteinase 9, Neovascularization, Pathologic, Phosphatidylinositol 3-Kinases, Phosphorylation, Proto-Oncogene Proteins c-akt, STAT3 Transcription Factor, Signal Transduction.
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Does curcumin suppress vasculogenic mimicry capacity of hepatocellular carcinoma cells through STAT3 and PI3K/AKT inhibition? Context: Vasculogenic mimicry (VM) refers to the process in which highly invasive cancer cells mimic endothelial cells by forming blood channels. In the present study, we investigated the effect of curcumin, a natural product from turmeric, on VM of SK-Hep-1 human hepatocellular carcinoma (HCC) cells. In vitro VM, cell migration, and matrix metalloproteinase-9 (MMP9) production of HCC cells were determined by Matrigel tube formation assay, Transwell cell migration assay, and gelatin zymography, respectively. Effects of curcumin on AKT, signal transducer and activator of transcription 3 (STAT3), extracellular signal-regulated kinase (ERK) and nuclear factor-κB (NF-κB) signaling pathways were determined by immunoblot analysis. At non-cytotoxic concentrations, curcumin inhibited VM, reduced cell migration and MMP9 production of the HCC cells. Further study revealed that the anti-VM effect of curcumin was due to inhibition of AKT and STAT3 phosphorylation, as confirmed by specific inhibitors.
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Curcumin presents proven potential as an anti-VM agent in HCC cells, through down-regulation of STAT3 and AKT signaling pathways. Final Decision: yes