Publications by authors named "Chao-shen Huang-Fu"
Article Synopsis
- This study investigates how sodium nitrite affects reactive oxygen species (ROS) and promotes epithelial-mesenchymal transition (EMT) in hepatoma cells within mice.
- The research involved injecting H22 liver cancer cells into mice and administering varying doses of sodium nitrite over 21 days to analyze changes in tumor characteristics and oxidative stress markers.
- Findings revealed that sodium nitrite treatment led to increased ROS levels, enhanced EMT indicators (like HIF-1alpha and vimentin), and reduced E-cadherin expression, indicating a link between sodium nitrite, ROS signaling, and tumor aggressiveness.
To investigate the potential ability of the nitrite to induce neuronal differentiation of PC12 cells, cultured PC12 cells planted on matrigel in the presence or absence of sodium nitrite were employed as model, nerve growth factor (NGF) served as a positive control. After 48 h, sodium nitrite enhanced cell viability and vascular endothelial growth factor (VEGF) secretion. Same as the effect of NGF, sodium nitrite (1.
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- - The study investigates the cytotoxic effects of a new antibacterial compound, piperonal ciprofloxacin hydrazone (QNT4), on human liver cancer cells (SMMC-7721) and other cancer cell lines, utilizing various assays to measure cell growth and apoptosis.
- - QNT4 effectively inhibited cancer cell proliferation in a dose- and time-dependent manner, with half-maximal inhibitory concentrations (IC50) calculated for SMMC-7721 (2.956 μmol/L), MCF-7, and HCT-8 cells.
- - The compound induced significant apoptosis in SMMC-7721 cells, demonstrated by increased apoptotic markers, altered mitochondrial function, and enhanced activity of proteins involved in apoptosis, such
This study is to find out the induction by sodium nitrite of epithelial-mesenchymal transition (EMT) in human hepatocellular carcinoma cells, SMMC-7721. After treatment of SMMC-7721 with 0.25 - 25 mmol.
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- The study investigates the effects of the compound FQ16 on the apoptosis of liver cancer cells (SMMC-7721) in lab conditions, focusing on different concentrations and treatment durations.
- FQ16 showed a dose-dependent inhibition of cell proliferation and significantly increased cell apoptosis, as indicated by various assays that measured DNA damage and mitochondrial membrane potential changes.
- The results revealed that FQ16 affected topoisomerase II activity and led to changes in the expression of key proteins and genes involved in apoptosis, including an increase in pro-apoptotic factors and a decrease in an anti-apoptotic factor.
Article Synopsis
- This study explores how NaNO2 preconditioning protects human liver cancer cells (SMMC-7721) from damage caused by ethanol exposure.
- Cells treated with NaNO2 showed reduced cell death and apoptosis when exposed to ethanol, suggesting a protective effect.
- The protective mechanism is linked to increased levels of HIF-1alpha and Bcl-2, alongside decreased levels of pro-apoptotic proteins like Bax and Caspase-3, indicating a complex interaction at the cellular level.