Luteolin inhibits proliferation of lung cancer A549 cells by increasing ROS production and inhibiting the AKT/mTOR signaling pathway and HO-1 expression

• Published in: Nan fang yi ke da xue xue bao = Journal of Southern Medical University 2024-12, Vol.44 (12), p.2367
• Main Authors: Li, Huan, Qiu, Zixin, Xu, Wenjie, Chen, Xue, Wei, Diandian, Wang, Yun
• Format: Article
• Language: Chinese
• Subjects: A549 Cells; Apoptosis - drug effects; Autophagy - drug effects; Cell Proliferation - drug effects; Cell Survival - drug effects; Heme Oxygenase-1 - metabolism; Humans; Lung Neoplasms - metabolism; Lung Neoplasms - pathology; Luteolin - pharmacology; Proto-Oncogene Proteins c-akt - metabolism; Reactive Oxygen Species - metabolism; Signal Transduction - drug effects; TOR Serine-Threonine Kinases - metabolism
• ISSN: 1673-4254
• DOI: 10.12122/j.issn.1673-4254.2024.12.12

To investigate the mechanism of luteolin for inhibiting proliferation of lung cancer A549 cells. A549 cells treated with different concentrations of luteolin for 48 h were evaluated for changes in cell viability, proliferation, reactive oxygen species (ROS) production and apoptosis using MTT assay, plate cloning assay, EdU staining, DCFH-DA assay and Hoechst33258 staining. The changes in cell autophagy were examined with MDC staining, and the expressions of apoptosis-related proteins (Bax, Bcl-2, and cleaved caspase-9), autophagy-related proteins (LC3B, Beclin 1, and P62), AKT/mTOR pathway proteins, and HO-1 protein were detected using Western blotting. Treatment with luteolin dose-dependently inhibited the viability and proliferation of A549 cells, increased intracellular ROS levels, up-regulated the expressions of Bax, cleaved caspase-9, and Beclin 1, increased the LC3B-II/LC3B-I ratio, down-regulated the expressions of Bcl-2 and P62, and induced cell apoptosis and autophagy. Luteolin also significantly inh