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a , MAGL inhibitors identified from a viability-based chemical screen reduced HT-1080 cell viability; this effect was reversed by ferrostatin-1 (Fer-1, 5 µM). b , Schematic illustration of the lipolysis pathway highlighting ATGL-, DAGL- and MAGL-mediated DAG metabolism. c , Cell viability of HT-1080 cells with or without CRISPR–Cas9-mediated knockout of MAGL or ATGL (two independent sgRNAs each) treated with increasing concentrations of RSL3 or erastin for 24 h. d , Lipid peroxidation levels in ATGL-knockout HT-1080 cells treated with DMSO, RSL3 (20 nM) or erastin (10 µM) for 4 h. e , Cell viability of HT-1080 cells with or without DAGLA or DAGLB knockout treated with increasing concentrations of RSL3 or erastin for 24 h. f , Lipid peroxidation levels in HT-1080 cells with or without DAGLA or DAGLB knockout following treatment with DMSO, RSL3 (10 nM) or erastin (5 µM) for 4 h. g , Cell viability of HT-1080 cells treated with increasing concentrations of DO34 or KT109 for 24 h in the presence of DMSO, Fer-1 (5 <t>µM),</t> <t>necrostatin-1</t> (Nec-1, 10 µM) or Z-VAD-FMK (Z-VAD, 10 µM). h , Lipidomics profiling of DAG species in HT-1080 cells after treatment with DMSO or DO34 (20 µM, 12 h). i , Representative transmission electron microscopy images showing mitochondrial morphology in HT-1080 cells treated with DMSO, DO34 or KT109 (20 µM) for 4 h in the presence or absence of Fer-1 (5 µM). Scale bar, 2 µm. j , Cell viability of ATGL-knockout HT-1080 cells treated with increasing concentrations of DO34 or KT109 for 24 h. Data in c–h and j are mean ±s.d. from three biological replicates (n = 3). Statistical analysis in d , f and h was performed using one-way ANOVA; *P < 0.05, **P < 0.01, ***P < 0.001.
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Image Search Results


Representative PD-L1 immunohistochemical images showing high expression (CPS=80). The brown DAB staining indicates PD-L1 expression on the cell membrane, while blue hematoxylin counterstain marks the nuclei (magnification, ×200; scale bar, 100 µm).

Journal: Oncology Letters

Article Title: Long survival of PD-L1-positive mediastinal sarcomatoid carcinoma after immunotherapy and anti-angiogenic target therapy: A case report

doi: 10.3892/ol.2026.15690

Figure Lengend Snippet: Representative PD-L1 immunohistochemical images showing high expression (CPS=80). The brown DAB staining indicates PD-L1 expression on the cell membrane, while blue hematoxylin counterstain marks the nuclei (magnification, ×200; scale bar, 100 µm).

Article Snippet: The specimen obtained via bronchoscopy was sent to Amoy Diagnostics Co., Ltd. for genomic and programmed cell death ligand 1 (PD-L1) testing; no pathogenic gene mutations were detected.

Techniques: Immunohistochemical staining, Expressing, Staining, Membrane

a , MAGL inhibitors identified from a viability-based chemical screen reduced HT-1080 cell viability; this effect was reversed by ferrostatin-1 (Fer-1, 5 µM). b , Schematic illustration of the lipolysis pathway highlighting ATGL-, DAGL- and MAGL-mediated DAG metabolism. c , Cell viability of HT-1080 cells with or without CRISPR–Cas9-mediated knockout of MAGL or ATGL (two independent sgRNAs each) treated with increasing concentrations of RSL3 or erastin for 24 h. d , Lipid peroxidation levels in ATGL-knockout HT-1080 cells treated with DMSO, RSL3 (20 nM) or erastin (10 µM) for 4 h. e , Cell viability of HT-1080 cells with or without DAGLA or DAGLB knockout treated with increasing concentrations of RSL3 or erastin for 24 h. f , Lipid peroxidation levels in HT-1080 cells with or without DAGLA or DAGLB knockout following treatment with DMSO, RSL3 (10 nM) or erastin (5 µM) for 4 h. g , Cell viability of HT-1080 cells treated with increasing concentrations of DO34 or KT109 for 24 h in the presence of DMSO, Fer-1 (5 µM), necrostatin-1 (Nec-1, 10 µM) or Z-VAD-FMK (Z-VAD, 10 µM). h , Lipidomics profiling of DAG species in HT-1080 cells after treatment with DMSO or DO34 (20 µM, 12 h). i , Representative transmission electron microscopy images showing mitochondrial morphology in HT-1080 cells treated with DMSO, DO34 or KT109 (20 µM) for 4 h in the presence or absence of Fer-1 (5 µM). Scale bar, 2 µm. j , Cell viability of ATGL-knockout HT-1080 cells treated with increasing concentrations of DO34 or KT109 for 24 h. Data in c–h and j are mean ±s.d. from three biological replicates (n = 3). Statistical analysis in d , f and h was performed using one-way ANOVA; *P < 0.05, **P < 0.01, ***P < 0.001.

Journal: bioRxiv

Article Title: CHPT1–LCAT rewires lipolysis towards ferroptosis

doi: 10.64898/2026.03.15.711301

Figure Lengend Snippet: a , MAGL inhibitors identified from a viability-based chemical screen reduced HT-1080 cell viability; this effect was reversed by ferrostatin-1 (Fer-1, 5 µM). b , Schematic illustration of the lipolysis pathway highlighting ATGL-, DAGL- and MAGL-mediated DAG metabolism. c , Cell viability of HT-1080 cells with or without CRISPR–Cas9-mediated knockout of MAGL or ATGL (two independent sgRNAs each) treated with increasing concentrations of RSL3 or erastin for 24 h. d , Lipid peroxidation levels in ATGL-knockout HT-1080 cells treated with DMSO, RSL3 (20 nM) or erastin (10 µM) for 4 h. e , Cell viability of HT-1080 cells with or without DAGLA or DAGLB knockout treated with increasing concentrations of RSL3 or erastin for 24 h. f , Lipid peroxidation levels in HT-1080 cells with or without DAGLA or DAGLB knockout following treatment with DMSO, RSL3 (10 nM) or erastin (5 µM) for 4 h. g , Cell viability of HT-1080 cells treated with increasing concentrations of DO34 or KT109 for 24 h in the presence of DMSO, Fer-1 (5 µM), necrostatin-1 (Nec-1, 10 µM) or Z-VAD-FMK (Z-VAD, 10 µM). h , Lipidomics profiling of DAG species in HT-1080 cells after treatment with DMSO or DO34 (20 µM, 12 h). i , Representative transmission electron microscopy images showing mitochondrial morphology in HT-1080 cells treated with DMSO, DO34 or KT109 (20 µM) for 4 h in the presence or absence of Fer-1 (5 µM). Scale bar, 2 µm. j , Cell viability of ATGL-knockout HT-1080 cells treated with increasing concentrations of DO34 or KT109 for 24 h. Data in c–h and j are mean ±s.d. from three biological replicates (n = 3). Statistical analysis in d , f and h was performed using one-way ANOVA; *P < 0.05, **P < 0.01, ***P < 0.001.

Article Snippet: Cell death pathway inhibitors necrostatin-1 (MCE, cat. no. HY-15760) and Z-VAD-FMK (MCE, cat. no. HY-16658B) were used where indicated.

Techniques: CRISPR, Knock-Out, Transmission Assay, Electron Microscopy