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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: OBJECTIVE, METHODS, RESULTS. Meshes: Adenocarcinoma, Adenocarcinoma of Lung, Blotting, Western, Cell Line, Tumor, Cell Survival, Cells, Cultured, Chromatin Immunoprecipitation, DNA-Binding Proteins, Electrophoretic Mobility Shift Assay, Epithelial-Mesenchymal Transition, Expectorants, Fluorescent Antibody Technique, Indirect, Gene Expression Regulation, Neoplastic, Humans, Indicators and Reagents, Lung Neoplasms, Luteolin, NF-kappa B, Oncogene Protein v-akt, Phosphatidylinositol 3-Kinases, Real-Time Polymerase Chain Reaction, Signal Transduction, Snail Family Transcription Factors, Transcription Factors, Transforming Growth Factor beta1.
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Does luteolin attenuate TGF-β1-induced epithelial-mesenchymal transition of lung cancer cells by interfering in the PI3K/Akt-NF-κB-Snail pathway? Context: Luteolin is a natural flavonoid that possesses a variety of pharmacological activities, such as anti-inflammatory and anti-cancer abilities. Whether luteolin regulates the transformation ability of lung cancer cells remains unclear. The current study aims to uncover the effects and underlying mechanisms of luteolin in regulation of and epithelial-mesenchymal transition of lung cancer cells. The lung adenocarcinoma A549 cells were used in this experiment; the cells were pretreated with luteolin followed by administration with TGF-β1. The expression levels of various cadherin and related upstream regulatory modules were examined. Pretreatment of luteolin prevented the morphological change and downregulation of E-cadherin of A549 cells induced by TGF-β1. In addition, the activation of PI3K-Akt-IκBa-NF-κB-Snail pathway which leads to the decline of E-cadherin induced by TGF-β1 was also attenuated under the pretreatment of luteolin.
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We provide the mechanisms about how luteolin attenuated the epithelial-mesenchymal transition of A549 lung cancer cells induced by TGF-β1. This finding will strengthen the anti-cancer effects of flavonoid compounds via the regulation of migration/invasion and EMT ability of various cancer cells. Final Decision: yes