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Fig. 5 — A novel derivative of valepotriate inhibits the PI3K/AKT pathway and causes Noxa
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Created: 2026-04-21T18:29:40
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Fig. 5Figure 5
Amcp disrupted the mitochondrial membrane potential and affected mitochondrial proteins. a BxPC-3 and SW1990 cells were seeded into six-well plates at a density of 2 × 10 5 /well and were cultured for 24 h. After treatment with Amcp for 12 h, JC-1 staining was used to observe the depolarized mitochondrial membrane potential. Cells were analyzed by flow cytometry. b Quantitative analysis of cells with a depolarized mitochondria membrane. c Cells were treated with the indicated concentrations of Amcp or gemcitabine (Gem) for 24 h before Western blotting assays. * P < 0.05. d The protein level of Noxa was dramatically reduced by Noxa siRNA knockdown in BxPC-3 cells. e BxPC-3 cells were exposed to Amcp for 24 h with or without Noxa knockdown. Cell viability was determined by CCK-8 assays. f Noxa was knocked down by siRNA in BxPC-3 cells before treatment and cells were exposed to the indicated concentrations of Amcp or gemcitabine for 24 h before Western blotting analysis. g B
▸Metadata
| pmid | paper-8281d7c4ac82 |
| caption | Amcp disrupted the mitochondrial membrane potential and affected mitochondrial proteins. a BxPC-3 and SW1990 cells were seeded into six-well plates at a density of 2 × 10 5 /well and were cultured fo |
| image_url | https://www.ebi.ac.uk/europepmc/articles/PMC7470838/bin/41401_2019_354_Fig5_HTML.jpg |
| paper_title | A novel derivative of valepotriate inhibits the PI3K/AKT pathway and causes Noxa-dependent apoptosis in human pancreatic cancer cells. |
| figure_label | Fig. 5 |
| figure_number | 5 |
| _schema_version | 1 |
| source_strategy | pmc_api |
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