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Asaraldehyde inhibits malignant phenotypes of NSCLC through ferroptosis induction. A549 and H1299 cells were treated with various concentrations of Asaraldehyde for 48 h. A. Expression of ferroptosis-related proteins was detected by western blot. B. Intracellular <t>ROS</t> level was detected by DHE staining (magnification, ×100, Scale bar = 50 μm). C. Intracellular labile iron level was detected by FerroOrange staining. (magnification, ×630, Scale bar = 10 μm). D-F. Intracellular GSH, LPO and MDA level were detected by commercial kits. A549, HCC827, H292 and H1299 cells were treated with Asaraldehyde in the presence or absence of 10 µM Ferrostatin-1. G-J. Cell viability was examined by CCK-8 assay. K, L. Colony formation was examined by crystal violet staining. (magnification, ×1, Scale bar = 5 mm). M, N. Cell migration ability was examined by wound healing assay (magnification, ×50, Scale bar = 200 µm). Data were presented as mean ± SD. ns P > 0.05, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.
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Asaraldehyde inhibits malignant phenotypes of NSCLC through ferroptosis induction. A549 and H1299 cells were treated with various concentrations of Asaraldehyde for 48 h. A. Expression of ferroptosis-related proteins was detected by western blot. B. Intracellular <t>ROS</t> level was detected by DHE staining (magnification, ×100, Scale bar = 50 μm). C. Intracellular labile iron level was detected by FerroOrange staining. (magnification, ×630, Scale bar = 10 μm). D-F. Intracellular GSH, LPO and MDA level were detected by commercial kits. A549, HCC827, H292 and H1299 cells were treated with Asaraldehyde in the presence or absence of 10 µM Ferrostatin-1. G-J. Cell viability was examined by CCK-8 assay. K, L. Colony formation was examined by crystal violet staining. (magnification, ×1, Scale bar = 5 mm). M, N. Cell migration ability was examined by wound healing assay (magnification, ×50, Scale bar = 200 µm). Data were presented as mean ± SD. ns P > 0.05, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.
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Asaraldehyde inhibits malignant phenotypes of NSCLC through ferroptosis induction. A549 and H1299 cells were treated with various concentrations of Asaraldehyde for 48 h. A. Expression of ferroptosis-related proteins was detected by western blot. B. Intracellular <t>ROS</t> level was detected by DHE staining (magnification, ×100, Scale bar = 50 μm). C. Intracellular labile iron level was detected by FerroOrange staining. (magnification, ×630, Scale bar = 10 μm). D-F. Intracellular GSH, LPO and MDA level were detected by commercial kits. A549, HCC827, H292 and H1299 cells were treated with Asaraldehyde in the presence or absence of 10 µM Ferrostatin-1. G-J. Cell viability was examined by CCK-8 assay. K, L. Colony formation was examined by crystal violet staining. (magnification, ×1, Scale bar = 5 mm). M, N. Cell migration ability was examined by wound healing assay (magnification, ×50, Scale bar = 200 µm). Data were presented as mean ± SD. ns P > 0.05, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.
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Asaraldehyde inhibits malignant phenotypes of NSCLC through ferroptosis induction. A549 and H1299 cells were treated with various concentrations of Asaraldehyde for 48 h. A. Expression of ferroptosis-related proteins was detected by western blot. B. Intracellular <t>ROS</t> level was detected by DHE staining (magnification, ×100, Scale bar = 50 μm). C. Intracellular labile iron level was detected by FerroOrange staining. (magnification, ×630, Scale bar = 10 μm). D-F. Intracellular GSH, LPO and MDA level were detected by commercial kits. A549, HCC827, H292 and H1299 cells were treated with Asaraldehyde in the presence or absence of 10 µM Ferrostatin-1. G-J. Cell viability was examined by CCK-8 assay. K, L. Colony formation was examined by crystal violet staining. (magnification, ×1, Scale bar = 5 mm). M, N. Cell migration ability was examined by wound healing assay (magnification, ×50, Scale bar = 200 µm). Data were presented as mean ± SD. ns P > 0.05, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.
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Asaraldehyde inhibits malignant phenotypes of NSCLC through ferroptosis induction. A549 and H1299 cells were treated with various concentrations of Asaraldehyde for 48 h. A. Expression of ferroptosis-related proteins was detected by western blot. B. Intracellular ROS level was detected by DHE staining (magnification, ×100, Scale bar = 50 μm). C. Intracellular labile iron level was detected by FerroOrange staining. (magnification, ×630, Scale bar = 10 μm). D-F. Intracellular GSH, LPO and MDA level were detected by commercial kits. A549, HCC827, H292 and H1299 cells were treated with Asaraldehyde in the presence or absence of 10 µM Ferrostatin-1. G-J. Cell viability was examined by CCK-8 assay. K, L. Colony formation was examined by crystal violet staining. (magnification, ×1, Scale bar = 5 mm). M, N. Cell migration ability was examined by wound healing assay (magnification, ×50, Scale bar = 200 µm). Data were presented as mean ± SD. ns P > 0.05, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Journal: American Journal of Cancer Research

Article Title: Asaraldehyde suppresses non-small cell lung cancer progression via ferroptosis induction and inhibition of PI3K-AKT signaling

doi: 10.62347/UYNG3321

Figure Lengend Snippet: Asaraldehyde inhibits malignant phenotypes of NSCLC through ferroptosis induction. A549 and H1299 cells were treated with various concentrations of Asaraldehyde for 48 h. A. Expression of ferroptosis-related proteins was detected by western blot. B. Intracellular ROS level was detected by DHE staining (magnification, ×100, Scale bar = 50 μm). C. Intracellular labile iron level was detected by FerroOrange staining. (magnification, ×630, Scale bar = 10 μm). D-F. Intracellular GSH, LPO and MDA level were detected by commercial kits. A549, HCC827, H292 and H1299 cells were treated with Asaraldehyde in the presence or absence of 10 µM Ferrostatin-1. G-J. Cell viability was examined by CCK-8 assay. K, L. Colony formation was examined by crystal violet staining. (magnification, ×1, Scale bar = 5 mm). M, N. Cell migration ability was examined by wound healing assay (magnification, ×50, Scale bar = 200 µm). Data were presented as mean ± SD. ns P > 0.05, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Article Snippet: To assess reactive oxygen species (ROS) levels, cells were incubated with 5 μM Dihydroethidium (DHE; MedChemExpress, #HY-D0079) for 30 minutes at 37°C in the dark, then washed twice with PBS.

Techniques: Expressing, Western Blot, Staining, CCK-8 Assay, Migration, Wound Healing Assay