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Title:
Metformin induces ferroptosis through the Nrf2/HO-1 signaling in lung cancer | BMC Pulmonary Medicine
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Background Metformin is the most frequently prescribed medication for the treatment of type II diabetes mellitus and has played an anti-tumor potential in a variety of cancer types. Metformin can inhibit the growth of many cancer cells through various mechanisms, including ferroptosis. However, it is still unclear whether metformin can induce ferroptosis in lung cancer. Methods This study evaluated the anti-tumor effect of metformin by detecting the levels of oxidative stress factors, the levels of ferrous ions, and the expression of ferroptosis-related genes in A549 and H1299 lung cancer cell lines treated with or without metformin. Results The results showed that metformin treatment increased the levels of MDA, ROS and iron ions, while decreased the levels of GSH, T-SOD and CAT. Meanwhile, metformin treatment reduced the protein expression levels of Gpx4 and SLC7A11, Nrf2 and HO-1, while the addition of ferroptosis inhibitor ferrostatin-1 reversed the reduction. Conclusions These results demonstrated that metformin exerts anti-tumor effects by inducing ferroptosis through the Nrf2/HO-1 signaling pathway in lung cancer cells, providing a theoretical basis for drug therapy of lung cancer patients.
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Keywords {š}
cancer, metformin, lung, cells, ferroptosis, article, pubmed, cell, google, scholar, cas, expression, china, treatment, levels, assay, central, protein, cat, slca, data, signaling, mrna, fig, nrfho, results, reduced, gpx, death, nrf, patients, induces, ferrous, pathway, survival, oxidative, ros, gsh, inhibiting, significantly, control, group, liu, research, stress, treated, mda, iron, kit, concentration,
Topics {āļø}
regulating mir-365a-3p/nrf2 axis oxidative/antioxidative ferroptosis-relative factors targeting mir-324-3p/gpx4 axis goat anti-mouse igg small-cell lung cancer mir-324-3p/gpx4 axis nrf-2/ho-1 signaling axis nrf2/ho-1 signaling axis p62-keap1-nrf2 pathway [23] p62-keap1-nrf2 pathway cancer-related deaths worldwide heme-binding ferrous content rt-qpcr results showed newly identified iron-dependent nrf2/ho-1 signaling pathway metformin-induced ferroptosis remains full access article download pdf oxidative stress induced induced oxidative stress inhibit epithelial-mesenchymal transformation oxidative stress factors nonapoptotic cell death febs open bio apoptotic cell death related subjects inhibit ferroptosis-related molecules small-molecule inhibitor total superoxide dismutase induce oxidative stress ferroptosis inducers erastin cancer cell lines rt-qpcr results increasing oxidative stress cell death pathways rt-qpcr primers privacy choices/manage cookies cell death dis jie wu designed antioxidant gsh t-sod liver cancer cells nrf2/ho-1 signaling cancer cell killing tyrosine kinase receptors sorafenib induces ferroptosis methods cell lines mol cell biochem jie wu prepared assay buffer ii ros assay kit
Questions {ā}
- Metformin for Cardiovascular Protection, Inflammatory Bowel Disease, Osteoporosis, Periodontitis, Polycystic Ovarian Syndrome, Neurodegeneration, Cancer, Inflammation and Senescence: What Is Next?
- Will we unlock the benefit of Metformin for patients with Lung Cancer?
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headline:Metformin induces ferroptosis through the Nrf2/HO-1 signaling in lung cancer
description:Metformin is the most frequently prescribed medication for the treatment of type II diabetes mellitus and has played an anti-tumor potential in a variety of cancer types. Metformin can inhibit the growth of many cancer cells through various mechanisms, including ferroptosis. However, it is still unclear whether metformin can induce ferroptosis in lung cancer. This study evaluated the anti-tumor effect of metformin by detecting the levels of oxidative stress factors, the levels of ferrous ions, and the expression of ferroptosis-related genes in A549 and H1299 lung cancer cell lines treated with or without metformin. The results showed that metformin treatment increased the levels of MDA, ROS and iron ions, while decreased the levels of GSH, T-SOD and CAT. Meanwhile, metformin treatment reduced the protein expression levels of Gpx4 and SLC7A11, Nrf2 and HO-1, while the addition of ferroptosis inhibitor ferrostatin-1 reversed the reduction. These results demonstrated that metformin exerts anti-tumor effects by inducing ferroptosis through the Nrf2/HO-1 signaling pathway in lung cancer cells, providing a theoretical basis for drug therapy of lung cancer patients.
datePublished:2023-09-25T00:00:00Z
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Lung cancer
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Nrf2/HO-1 signaling
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headline:Metformin induces ferroptosis through the Nrf2/HO-1 signaling in lung cancer
description:Metformin is the most frequently prescribed medication for the treatment of type II diabetes mellitus and has played an anti-tumor potential in a variety of cancer types. Metformin can inhibit the growth of many cancer cells through various mechanisms, including ferroptosis. However, it is still unclear whether metformin can induce ferroptosis in lung cancer. This study evaluated the anti-tumor effect of metformin by detecting the levels of oxidative stress factors, the levels of ferrous ions, and the expression of ferroptosis-related genes in A549 and H1299 lung cancer cell lines treated with or without metformin. The results showed that metformin treatment increased the levels of MDA, ROS and iron ions, while decreased the levels of GSH, T-SOD and CAT. Meanwhile, metformin treatment reduced the protein expression levels of Gpx4 and SLC7A11, Nrf2 and HO-1, while the addition of ferroptosis inhibitor ferrostatin-1 reversed the reduction. These results demonstrated that metformin exerts anti-tumor effects by inducing ferroptosis through the Nrf2/HO-1 signaling pathway in lung cancer cells, providing a theoretical basis for drug therapy of lung cancer patients.
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