ArticleCancer medicine2026
Carnosic Acid Mediates Production of Reactive Oxygen Species to Regulate Mitogen-Activated Protein Kinase Pathway Phosphorylation and Induce Apoptosis in Human Breast Cancer Cells.
Article in Cancer medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
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7 authors.
Funding
Abstract
backgroundReactive oxygen species (ROS) can induce cancer cell apoptosis, which plays a crucial role in breast cancer therapy. Carnosic acid (CA) exerts an anti-tumor effect via generating ROS or activating the mitochondria-related apoptosis pathway in vitro and in vivo. The deoxy-glucose derivative CN5DG labeled with
methodsInhibition of cancer cell proliferation by CA was assessed by MTT and cell colony-formation assays. The mechanism of CA-induced cancer cell apoptosis was examined by western blotting and the apoptosis rate was detected by flow cytometry. The in vivo anti-tumor effect of CA was assessed by immunohistochemistry and
resultsCA promoted cancer cell apoptosis via ROS generation, which activated c-Jun N-terminal kinase (JNK) and p38 phosphorylation. The apoptosis rates of T47D and MCF7 cells treated with CA (IC50 concentration) for 24 h were 44.97% ± 1.56% and 39.74% ± 1.78%, respectively. The antioxidant N-acetyl-L-cysteine (5 μM) abolished CA-induced apoptosis. MCF-7 xenografts without CA were visualized in vivo at all time points by
conclusionCA can induce breast cancer apoptosis via ROS generation and activation of JNK and p38 phosphorylation. The anti-tumor effect of CA can be assessed using
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