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human cancer cell lines ht1080  (ATCC)


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    ATCC human cancer cell lines ht1080
    a, Schematic representation of the FSP1-dependent model used to identify factors supporting FSP1 function. Upper left: the primary protective system against lipid peroxidation (LPO) is the enzyme GPX4, complemented by FSP1. Lower left: cells treated with an FSP1 inhibitor (iFSP1) can rely on GPX4 activity to survive. Upper right: FSP1-dependent <t>HT1080</t> cells (HT1080 GPX4KO/FSP1OE ). In HT1080 cells, as in many others, knocking out GPX4 induces ferroptosis due to insufficient endogenous FSP1 levels to compensate for GPX4 loss. However, cell survival can be rescued by overexpressing FSP1. Lower right: Upon pharmacological inhibition of FSP1 (iFSP1 treatment), cells undergo ferroptosis as they solely rely on FSP1 function for survival. b , Immunoblot (IB) analysis of ACSL4, FSP1, GPX4, and vinculin in HT1080 parental and HT1080 GPX4KO/FSP1OE cells. c , Dose-dependent toxicity of an FSP1 inhibitor (iFSP1) in HT1080 parental and HT1080 GPX4KO/FSP1OE cell lines. Cell viability was monitored using Alamar blue after 24 h of treatment. Where indicated, cells were treated with the ferroptosis inhibitor Lip-1 (500 nM). d , Schematic representation of the screening strategy used to identify novel factors supporting FSP1 function in the previously-described FSP1-dependent cellular model (see ). HT1080 GPX4KO/FSP1OE cells were transduced with a gRNA library targeting approximately 3000 genes and selected over 7 days in the presence of the ferroptosis inhibitor Lip-1 (500 nM). Subsequently, cells proliferate with or without Lip-1 supplementation for additional 14 days. e, Graphical representation of the results from two independently performed CRISPR screens; plot depicts the score calculated using the MaGeCK package (x-axis) and the –Log false discovery rate (y-axis). Riboflavin kinase (RFK) and stearoyl-CoA desaturase-1 (SCD1) were identified as potentially robust candidates to modulate FSP1 function. f , Immunoblot (IB) analysis of RFK, FSP1, and vinculin in A375 cells transduced with either a non-targeting control (NT) or three different RFK-targeting sgRNAs. g , Dose-dependent toxicity of RSL3 and ML210 in A375 cells transduced with either a non-targeting control (NT) or three different RFK-targeting sgRNAs. Cell viability was monitored after 72 h of treatment.
    Human Cancer Cell Lines Ht1080, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 4159 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human cancer cell lines ht1080/product/ATCC
    Average 98 stars, based on 4159 article reviews
    human cancer cell lines ht1080 - by Bioz Stars, 2026-02
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    1) Product Images from "Riboflavin metabolism shapes FSP1-driven ferroptosis resistance"

    Article Title: Riboflavin metabolism shapes FSP1-driven ferroptosis resistance

    Journal: bioRxiv

    doi: 10.1101/2025.08.05.668651

    a, Schematic representation of the FSP1-dependent model used to identify factors supporting FSP1 function. Upper left: the primary protective system against lipid peroxidation (LPO) is the enzyme GPX4, complemented by FSP1. Lower left: cells treated with an FSP1 inhibitor (iFSP1) can rely on GPX4 activity to survive. Upper right: FSP1-dependent HT1080 cells (HT1080 GPX4KO/FSP1OE ). In HT1080 cells, as in many others, knocking out GPX4 induces ferroptosis due to insufficient endogenous FSP1 levels to compensate for GPX4 loss. However, cell survival can be rescued by overexpressing FSP1. Lower right: Upon pharmacological inhibition of FSP1 (iFSP1 treatment), cells undergo ferroptosis as they solely rely on FSP1 function for survival. b , Immunoblot (IB) analysis of ACSL4, FSP1, GPX4, and vinculin in HT1080 parental and HT1080 GPX4KO/FSP1OE cells. c , Dose-dependent toxicity of an FSP1 inhibitor (iFSP1) in HT1080 parental and HT1080 GPX4KO/FSP1OE cell lines. Cell viability was monitored using Alamar blue after 24 h of treatment. Where indicated, cells were treated with the ferroptosis inhibitor Lip-1 (500 nM). d , Schematic representation of the screening strategy used to identify novel factors supporting FSP1 function in the previously-described FSP1-dependent cellular model (see ). HT1080 GPX4KO/FSP1OE cells were transduced with a gRNA library targeting approximately 3000 genes and selected over 7 days in the presence of the ferroptosis inhibitor Lip-1 (500 nM). Subsequently, cells proliferate with or without Lip-1 supplementation for additional 14 days. e, Graphical representation of the results from two independently performed CRISPR screens; plot depicts the score calculated using the MaGeCK package (x-axis) and the –Log false discovery rate (y-axis). Riboflavin kinase (RFK) and stearoyl-CoA desaturase-1 (SCD1) were identified as potentially robust candidates to modulate FSP1 function. f , Immunoblot (IB) analysis of RFK, FSP1, and vinculin in A375 cells transduced with either a non-targeting control (NT) or three different RFK-targeting sgRNAs. g , Dose-dependent toxicity of RSL3 and ML210 in A375 cells transduced with either a non-targeting control (NT) or three different RFK-targeting sgRNAs. Cell viability was monitored after 72 h of treatment.
    Figure Legend Snippet: a, Schematic representation of the FSP1-dependent model used to identify factors supporting FSP1 function. Upper left: the primary protective system against lipid peroxidation (LPO) is the enzyme GPX4, complemented by FSP1. Lower left: cells treated with an FSP1 inhibitor (iFSP1) can rely on GPX4 activity to survive. Upper right: FSP1-dependent HT1080 cells (HT1080 GPX4KO/FSP1OE ). In HT1080 cells, as in many others, knocking out GPX4 induces ferroptosis due to insufficient endogenous FSP1 levels to compensate for GPX4 loss. However, cell survival can be rescued by overexpressing FSP1. Lower right: Upon pharmacological inhibition of FSP1 (iFSP1 treatment), cells undergo ferroptosis as they solely rely on FSP1 function for survival. b , Immunoblot (IB) analysis of ACSL4, FSP1, GPX4, and vinculin in HT1080 parental and HT1080 GPX4KO/FSP1OE cells. c , Dose-dependent toxicity of an FSP1 inhibitor (iFSP1) in HT1080 parental and HT1080 GPX4KO/FSP1OE cell lines. Cell viability was monitored using Alamar blue after 24 h of treatment. Where indicated, cells were treated with the ferroptosis inhibitor Lip-1 (500 nM). d , Schematic representation of the screening strategy used to identify novel factors supporting FSP1 function in the previously-described FSP1-dependent cellular model (see ). HT1080 GPX4KO/FSP1OE cells were transduced with a gRNA library targeting approximately 3000 genes and selected over 7 days in the presence of the ferroptosis inhibitor Lip-1 (500 nM). Subsequently, cells proliferate with or without Lip-1 supplementation for additional 14 days. e, Graphical representation of the results from two independently performed CRISPR screens; plot depicts the score calculated using the MaGeCK package (x-axis) and the –Log false discovery rate (y-axis). Riboflavin kinase (RFK) and stearoyl-CoA desaturase-1 (SCD1) were identified as potentially robust candidates to modulate FSP1 function. f , Immunoblot (IB) analysis of RFK, FSP1, and vinculin in A375 cells transduced with either a non-targeting control (NT) or three different RFK-targeting sgRNAs. g , Dose-dependent toxicity of RSL3 and ML210 in A375 cells transduced with either a non-targeting control (NT) or three different RFK-targeting sgRNAs. Cell viability was monitored after 72 h of treatment.

    Techniques Used: Activity Assay, Inhibition, Western Blot, Transduction, CRISPR, Control

    a , Volcano plot of quantified proteins showing their change in A375 parental cells cultured in riboflavin-deficient medium for 96 h. Proteins are plotted based on their fold change (FC: riboflavin deficient/normal). b , Immunoblot (IB) analysis of FSP1, GPX4, and vinculin in HT1080, A375, MDA-MB-231, and A549 parental cell lines after 96 h of growth in riboflavin-deficient medium or medium supplemented with 1 µM riboflavin. c , Lipid peroxidation evaluated by C11-BODIPY 581/591 staining of A375 parental cell line cultured for 72 h in riboflavin-deficient medium or medium supplemented with 1 µM riboflavin and after treatment with DMSO, RSL3 (200 nM), or RSL3 (200 nM) + Lip-1 (500 nM) for 6 h. d , Dose-dependent toxicity of RSL3 in the absence or presence of an FSP1 inhibitor (iFSP1 3 µM) in HT1080, A375, MDA-MB-231, and A549 parental cell lines pre-cultured in riboflavin-deficient medium or medium supplemented with 1 µM riboflavin for 48 h. Cell viability was monitored using Alamar blue after 96 h of treatment. e , Dose-dependent toxicity of RSL3 in the absence or presence of an FSP1 inhibitor (iFSP1 3 µM) in A375 and MDA-MB-231 cells transduced with either a non-targeting control (NT) or an FSP1-targeting sgRNAs pre-cultured in riboflavin-deficient medium or medium supplemented with 1 µM riboflavin for 48 h. Cell viability was monitored after 96 h of treatment. f , Immunoblot (IB) analysis of ACSL4, FSP1, NQO1, and vinculin in A375 and MDA-MB-231 cells transduced with either a non-targeting control (NT) or an FSP1-targeting sgRNAs cultured in riboflavin-deficient medium or medium supplemented with 1 µM riboflavin for 96 h. g , Epilipidomics analysis of A375 parental cells pre-cultured in riboflavin-deficient medium or medium supplemented with 1 µM riboflavin for 72 h after treatment with DMSO, RSL3 (200 nM), or RSL3 (200 nM) + Lip-1 (500 nM) for 6 h.
    Figure Legend Snippet: a , Volcano plot of quantified proteins showing their change in A375 parental cells cultured in riboflavin-deficient medium for 96 h. Proteins are plotted based on their fold change (FC: riboflavin deficient/normal). b , Immunoblot (IB) analysis of FSP1, GPX4, and vinculin in HT1080, A375, MDA-MB-231, and A549 parental cell lines after 96 h of growth in riboflavin-deficient medium or medium supplemented with 1 µM riboflavin. c , Lipid peroxidation evaluated by C11-BODIPY 581/591 staining of A375 parental cell line cultured for 72 h in riboflavin-deficient medium or medium supplemented with 1 µM riboflavin and after treatment with DMSO, RSL3 (200 nM), or RSL3 (200 nM) + Lip-1 (500 nM) for 6 h. d , Dose-dependent toxicity of RSL3 in the absence or presence of an FSP1 inhibitor (iFSP1 3 µM) in HT1080, A375, MDA-MB-231, and A549 parental cell lines pre-cultured in riboflavin-deficient medium or medium supplemented with 1 µM riboflavin for 48 h. Cell viability was monitored using Alamar blue after 96 h of treatment. e , Dose-dependent toxicity of RSL3 in the absence or presence of an FSP1 inhibitor (iFSP1 3 µM) in A375 and MDA-MB-231 cells transduced with either a non-targeting control (NT) or an FSP1-targeting sgRNAs pre-cultured in riboflavin-deficient medium or medium supplemented with 1 µM riboflavin for 48 h. Cell viability was monitored after 96 h of treatment. f , Immunoblot (IB) analysis of ACSL4, FSP1, NQO1, and vinculin in A375 and MDA-MB-231 cells transduced with either a non-targeting control (NT) or an FSP1-targeting sgRNAs cultured in riboflavin-deficient medium or medium supplemented with 1 µM riboflavin for 96 h. g , Epilipidomics analysis of A375 parental cells pre-cultured in riboflavin-deficient medium or medium supplemented with 1 µM riboflavin for 72 h after treatment with DMSO, RSL3 (200 nM), or RSL3 (200 nM) + Lip-1 (500 nM) for 6 h.

    Techniques Used: Cell Culture, Western Blot, Staining, Transduction, Control

    a , Immunoblot (IB) analysis of FSP1, GPX4 and vinculin in HT1080, A375, MDA-MB-231 and 549 parental cell lines after 24, 48 and 144 h of growth in riboflavin-deficient medium or supplemented with 1 µM of riboflavin. b , Volcano plots of quantified proteins showing their change in A375 parental cells cultured in riboflavin-deficient medium for 24, 48 and 144 h. Proteins are plotted based on their fold change (FC: riboflavin deficient/normal). c , Heatmaps of quantified proteins showing their change in A375 parental cells cultured in riboflavin-deficient medium for 24, 48, 96 and 144 h (FC: riboflavin deficient/normal). d , Volcano plot of quantified flavoproteins showing their change in A375 parental cells cultured in riboflavin-deficient medium for 96 h (FC: riboflavin deficient/normal). e , Heatmap of quantified flavoproteins showing their change in A375 parental cells cultured in riboflavin-deficient medium for 96 h (FC: riboflavin deficient/normal). f , Lipid peroxidation evaluated by C11-BODIPY 581/591 staining of A375 parental cell line cultured for 72 h in riboflavin-deficient medium or supplemented with 1 µM of riboflavin and after treatment with DMSO, RSL3 (200 nM) or RSL3 (200 nM) + Lip-1 (500 nM) for 6 h. g , Dose-dependent toxicity of RSL3 in the presence of Lip-1 (500 nM) and iFSP1 (3 µM, when indicated) in HT1080, A375, MDA-MB-231 and A549 parental cell lines cultured in riboflavin-deficient medium or supplemented with 1 µM of riboflavin for 48 h. Cell viability was monitored using Alamar blue after 96 h of treatment. h , Absorbance at 517 nm corresponding to the radical initiator 2,2-diphenyl-1-picrylhydrazyl (DPPH) co-incubated with ferrostatin-1 (Fer-1), riboflavin (RbF) or roseoflavin (RoF) (n = 3). Data plotted are mean ± SD. Statistical significance was determined by one-way ANOVA followed by Dunnett’s multiple comparison test.
    Figure Legend Snippet: a , Immunoblot (IB) analysis of FSP1, GPX4 and vinculin in HT1080, A375, MDA-MB-231 and 549 parental cell lines after 24, 48 and 144 h of growth in riboflavin-deficient medium or supplemented with 1 µM of riboflavin. b , Volcano plots of quantified proteins showing their change in A375 parental cells cultured in riboflavin-deficient medium for 24, 48 and 144 h. Proteins are plotted based on their fold change (FC: riboflavin deficient/normal). c , Heatmaps of quantified proteins showing their change in A375 parental cells cultured in riboflavin-deficient medium for 24, 48, 96 and 144 h (FC: riboflavin deficient/normal). d , Volcano plot of quantified flavoproteins showing their change in A375 parental cells cultured in riboflavin-deficient medium for 96 h (FC: riboflavin deficient/normal). e , Heatmap of quantified flavoproteins showing their change in A375 parental cells cultured in riboflavin-deficient medium for 96 h (FC: riboflavin deficient/normal). f , Lipid peroxidation evaluated by C11-BODIPY 581/591 staining of A375 parental cell line cultured for 72 h in riboflavin-deficient medium or supplemented with 1 µM of riboflavin and after treatment with DMSO, RSL3 (200 nM) or RSL3 (200 nM) + Lip-1 (500 nM) for 6 h. g , Dose-dependent toxicity of RSL3 in the presence of Lip-1 (500 nM) and iFSP1 (3 µM, when indicated) in HT1080, A375, MDA-MB-231 and A549 parental cell lines cultured in riboflavin-deficient medium or supplemented with 1 µM of riboflavin for 48 h. Cell viability was monitored using Alamar blue after 96 h of treatment. h , Absorbance at 517 nm corresponding to the radical initiator 2,2-diphenyl-1-picrylhydrazyl (DPPH) co-incubated with ferrostatin-1 (Fer-1), riboflavin (RbF) or roseoflavin (RoF) (n = 3). Data plotted are mean ± SD. Statistical significance was determined by one-way ANOVA followed by Dunnett’s multiple comparison test.

    Techniques Used: Western Blot, Cell Culture, Staining, Incubation, Comparison

    a , Schematic representation of the metabolism of riboflavin (RbF) and its analog roseoflavin (RoF) by riboflavin kinase (encoded by RFK ) and FAD synthase (encoded by FLAD1 ). b , Dose-dependent toxicity of roseoflavin (RoF) and iFSP1 in the absence or presence of Lip-1 (500 nM) in HT1080 GPX4KO/FSP1OE . Cell viability was monitored using Alamar blue after 48 h of treatment. Cells were cultured in low-riboflavin medium (20 nM). c , Dose-dependent toxicity of the GPX4 inhibitor ML210 in A375 cells transduced with either a non-targeting control (NT) or a FSP1-targeting sgRNAs (FSP1 KO ) that were pre-treated with roseoflavin (RoF, 1, 3, and 10 nM) for 48 h. Cell viability was monitored after 48 h of ML210 treatment. Cells were cultured in low-riboflavin medium (20 nM). d , Immunoblot analysis (IB) of FSP1, NQO1, ACSL4, GPX4, and vinculin treated with roseoflavin (RoF 0, 20, 100, and 1000 nM) for 96 h in the absence or presence of riboflavin (RbF 20 nM). e , Dose-dependent toxicity of the GPX4 inhibitor ML210 in HT1080, MDA-MB-436, PC-9, and H460 parental cell lines pre-treated with roseoflavin (RoF, 1, 3, and 10 nM) for 48 h. Cell viability was monitored after 48 h of ML210 treatment. f , Immunoblot (IB) analysis of FSP1, NQO1, and vinculin in HT1080, MDA-MB-436, PC9, and H460 parental cell lines treated with roseoflavin (RoF, 20 nM) for 48 h in the absence or presence of riboflavin (RbF 20 nM). g , Riboflavin metabolism supports FSP1 function and promotes ferroptosis resistance. This is therefore a process that riboflavin analogs, such as roseoflavin can modulate.
    Figure Legend Snippet: a , Schematic representation of the metabolism of riboflavin (RbF) and its analog roseoflavin (RoF) by riboflavin kinase (encoded by RFK ) and FAD synthase (encoded by FLAD1 ). b , Dose-dependent toxicity of roseoflavin (RoF) and iFSP1 in the absence or presence of Lip-1 (500 nM) in HT1080 GPX4KO/FSP1OE . Cell viability was monitored using Alamar blue after 48 h of treatment. Cells were cultured in low-riboflavin medium (20 nM). c , Dose-dependent toxicity of the GPX4 inhibitor ML210 in A375 cells transduced with either a non-targeting control (NT) or a FSP1-targeting sgRNAs (FSP1 KO ) that were pre-treated with roseoflavin (RoF, 1, 3, and 10 nM) for 48 h. Cell viability was monitored after 48 h of ML210 treatment. Cells were cultured in low-riboflavin medium (20 nM). d , Immunoblot analysis (IB) of FSP1, NQO1, ACSL4, GPX4, and vinculin treated with roseoflavin (RoF 0, 20, 100, and 1000 nM) for 96 h in the absence or presence of riboflavin (RbF 20 nM). e , Dose-dependent toxicity of the GPX4 inhibitor ML210 in HT1080, MDA-MB-436, PC-9, and H460 parental cell lines pre-treated with roseoflavin (RoF, 1, 3, and 10 nM) for 48 h. Cell viability was monitored after 48 h of ML210 treatment. f , Immunoblot (IB) analysis of FSP1, NQO1, and vinculin in HT1080, MDA-MB-436, PC9, and H460 parental cell lines treated with roseoflavin (RoF, 20 nM) for 48 h in the absence or presence of riboflavin (RbF 20 nM). g , Riboflavin metabolism supports FSP1 function and promotes ferroptosis resistance. This is therefore a process that riboflavin analogs, such as roseoflavin can modulate.

    Techniques Used: Cell Culture, Transduction, Control, Western Blot



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    a, Schematic representation of the FSP1-dependent model used to identify factors supporting FSP1 function. Upper left: the primary protective system against lipid peroxidation (LPO) is the enzyme GPX4, complemented by FSP1. Lower left: cells treated with an FSP1 inhibitor (iFSP1) can rely on GPX4 activity to survive. Upper right: FSP1-dependent <t>HT1080</t> cells (HT1080 GPX4KO/FSP1OE ). In HT1080 cells, as in many others, knocking out GPX4 induces ferroptosis due to insufficient endogenous FSP1 levels to compensate for GPX4 loss. However, cell survival can be rescued by overexpressing FSP1. Lower right: Upon pharmacological inhibition of FSP1 (iFSP1 treatment), cells undergo ferroptosis as they solely rely on FSP1 function for survival. b , Immunoblot (IB) analysis of ACSL4, FSP1, GPX4, and vinculin in HT1080 parental and HT1080 GPX4KO/FSP1OE cells. c , Dose-dependent toxicity of an FSP1 inhibitor (iFSP1) in HT1080 parental and HT1080 GPX4KO/FSP1OE cell lines. Cell viability was monitored using Alamar blue after 24 h of treatment. Where indicated, cells were treated with the ferroptosis inhibitor Lip-1 (500 nM). d , Schematic representation of the screening strategy used to identify novel factors supporting FSP1 function in the previously-described FSP1-dependent cellular model (see ). HT1080 GPX4KO/FSP1OE cells were transduced with a gRNA library targeting approximately 3000 genes and selected over 7 days in the presence of the ferroptosis inhibitor Lip-1 (500 nM). Subsequently, cells proliferate with or without Lip-1 supplementation for additional 14 days. e, Graphical representation of the results from two independently performed CRISPR screens; plot depicts the score calculated using the MaGeCK package (x-axis) and the –Log false discovery rate (y-axis). Riboflavin kinase (RFK) and stearoyl-CoA desaturase-1 (SCD1) were identified as potentially robust candidates to modulate FSP1 function. f , Immunoblot (IB) analysis of RFK, FSP1, and vinculin in A375 cells transduced with either a non-targeting control (NT) or three different RFK-targeting sgRNAs. g , Dose-dependent toxicity of RSL3 and ML210 in A375 cells transduced with either a non-targeting control (NT) or three different RFK-targeting sgRNAs. Cell viability was monitored after 72 h of treatment.
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    a, Schematic representation of the FSP1-dependent model used to identify factors supporting FSP1 function. Upper left: the primary protective system against lipid peroxidation (LPO) is the enzyme GPX4, complemented by FSP1. Lower left: cells treated with an FSP1 inhibitor (iFSP1) can rely on GPX4 activity to survive. Upper right: FSP1-dependent <t>HT1080</t> cells (HT1080 GPX4KO/FSP1OE ). In HT1080 cells, as in many others, knocking out GPX4 induces ferroptosis due to insufficient endogenous FSP1 levels to compensate for GPX4 loss. However, cell survival can be rescued by overexpressing FSP1. Lower right: Upon pharmacological inhibition of FSP1 (iFSP1 treatment), cells undergo ferroptosis as they solely rely on FSP1 function for survival. b , Immunoblot (IB) analysis of ACSL4, FSP1, GPX4, and vinculin in HT1080 parental and HT1080 GPX4KO/FSP1OE cells. c , Dose-dependent toxicity of an FSP1 inhibitor (iFSP1) in HT1080 parental and HT1080 GPX4KO/FSP1OE cell lines. Cell viability was monitored using Alamar blue after 24 h of treatment. Where indicated, cells were treated with the ferroptosis inhibitor Lip-1 (500 nM). d , Schematic representation of the screening strategy used to identify novel factors supporting FSP1 function in the previously-described FSP1-dependent cellular model (see ). HT1080 GPX4KO/FSP1OE cells were transduced with a gRNA library targeting approximately 3000 genes and selected over 7 days in the presence of the ferroptosis inhibitor Lip-1 (500 nM). Subsequently, cells proliferate with or without Lip-1 supplementation for additional 14 days. e, Graphical representation of the results from two independently performed CRISPR screens; plot depicts the score calculated using the MaGeCK package (x-axis) and the –Log false discovery rate (y-axis). Riboflavin kinase (RFK) and stearoyl-CoA desaturase-1 (SCD1) were identified as potentially robust candidates to modulate FSP1 function. f , Immunoblot (IB) analysis of RFK, FSP1, and vinculin in A375 cells transduced with either a non-targeting control (NT) or three different RFK-targeting sgRNAs. g , Dose-dependent toxicity of RSL3 and ML210 in A375 cells transduced with either a non-targeting control (NT) or three different RFK-targeting sgRNAs. Cell viability was monitored after 72 h of treatment.
    Transfection Human Cancer Cell Lines Ht1080 Fibrosarcoma, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    rt pcr human cancer cell lines ht1080  (ATCC)
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    ATCC rt pcr human cancer cell lines ht1080
    a, Schematic representation of the FSP1-dependent model used to identify factors supporting FSP1 function. Upper left: the primary protective system against lipid peroxidation (LPO) is the enzyme GPX4, complemented by FSP1. Lower left: cells treated with an FSP1 inhibitor (iFSP1) can rely on GPX4 activity to survive. Upper right: FSP1-dependent <t>HT1080</t> cells (HT1080 GPX4KO/FSP1OE ). In HT1080 cells, as in many others, knocking out GPX4 induces ferroptosis due to insufficient endogenous FSP1 levels to compensate for GPX4 loss. However, cell survival can be rescued by overexpressing FSP1. Lower right: Upon pharmacological inhibition of FSP1 (iFSP1 treatment), cells undergo ferroptosis as they solely rely on FSP1 function for survival. b , Immunoblot (IB) analysis of ACSL4, FSP1, GPX4, and vinculin in HT1080 parental and HT1080 GPX4KO/FSP1OE cells. c , Dose-dependent toxicity of an FSP1 inhibitor (iFSP1) in HT1080 parental and HT1080 GPX4KO/FSP1OE cell lines. Cell viability was monitored using Alamar blue after 24 h of treatment. Where indicated, cells were treated with the ferroptosis inhibitor Lip-1 (500 nM). d , Schematic representation of the screening strategy used to identify novel factors supporting FSP1 function in the previously-described FSP1-dependent cellular model (see ). HT1080 GPX4KO/FSP1OE cells were transduced with a gRNA library targeting approximately 3000 genes and selected over 7 days in the presence of the ferroptosis inhibitor Lip-1 (500 nM). Subsequently, cells proliferate with or without Lip-1 supplementation for additional 14 days. e, Graphical representation of the results from two independently performed CRISPR screens; plot depicts the score calculated using the MaGeCK package (x-axis) and the –Log false discovery rate (y-axis). Riboflavin kinase (RFK) and stearoyl-CoA desaturase-1 (SCD1) were identified as potentially robust candidates to modulate FSP1 function. f , Immunoblot (IB) analysis of RFK, FSP1, and vinculin in A375 cells transduced with either a non-targeting control (NT) or three different RFK-targeting sgRNAs. g , Dose-dependent toxicity of RSL3 and ML210 in A375 cells transduced with either a non-targeting control (NT) or three different RFK-targeting sgRNAs. Cell viability was monitored after 72 h of treatment.
    Rt Pcr Human Cancer Cell Lines Ht1080, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rt pcr human cancer cell lines ht1080/product/ATCC
    Average 98 stars, based on 1 article reviews
    rt pcr human cancer cell lines ht1080 - by Bioz Stars, 2026-02
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    Image Search Results


    a, Schematic representation of the FSP1-dependent model used to identify factors supporting FSP1 function. Upper left: the primary protective system against lipid peroxidation (LPO) is the enzyme GPX4, complemented by FSP1. Lower left: cells treated with an FSP1 inhibitor (iFSP1) can rely on GPX4 activity to survive. Upper right: FSP1-dependent HT1080 cells (HT1080 GPX4KO/FSP1OE ). In HT1080 cells, as in many others, knocking out GPX4 induces ferroptosis due to insufficient endogenous FSP1 levels to compensate for GPX4 loss. However, cell survival can be rescued by overexpressing FSP1. Lower right: Upon pharmacological inhibition of FSP1 (iFSP1 treatment), cells undergo ferroptosis as they solely rely on FSP1 function for survival. b , Immunoblot (IB) analysis of ACSL4, FSP1, GPX4, and vinculin in HT1080 parental and HT1080 GPX4KO/FSP1OE cells. c , Dose-dependent toxicity of an FSP1 inhibitor (iFSP1) in HT1080 parental and HT1080 GPX4KO/FSP1OE cell lines. Cell viability was monitored using Alamar blue after 24 h of treatment. Where indicated, cells were treated with the ferroptosis inhibitor Lip-1 (500 nM). d , Schematic representation of the screening strategy used to identify novel factors supporting FSP1 function in the previously-described FSP1-dependent cellular model (see ). HT1080 GPX4KO/FSP1OE cells were transduced with a gRNA library targeting approximately 3000 genes and selected over 7 days in the presence of the ferroptosis inhibitor Lip-1 (500 nM). Subsequently, cells proliferate with or without Lip-1 supplementation for additional 14 days. e, Graphical representation of the results from two independently performed CRISPR screens; plot depicts the score calculated using the MaGeCK package (x-axis) and the –Log false discovery rate (y-axis). Riboflavin kinase (RFK) and stearoyl-CoA desaturase-1 (SCD1) were identified as potentially robust candidates to modulate FSP1 function. f , Immunoblot (IB) analysis of RFK, FSP1, and vinculin in A375 cells transduced with either a non-targeting control (NT) or three different RFK-targeting sgRNAs. g , Dose-dependent toxicity of RSL3 and ML210 in A375 cells transduced with either a non-targeting control (NT) or three different RFK-targeting sgRNAs. Cell viability was monitored after 72 h of treatment.

    Journal: bioRxiv

    Article Title: Riboflavin metabolism shapes FSP1-driven ferroptosis resistance

    doi: 10.1101/2025.08.05.668651

    Figure Lengend Snippet: a, Schematic representation of the FSP1-dependent model used to identify factors supporting FSP1 function. Upper left: the primary protective system against lipid peroxidation (LPO) is the enzyme GPX4, complemented by FSP1. Lower left: cells treated with an FSP1 inhibitor (iFSP1) can rely on GPX4 activity to survive. Upper right: FSP1-dependent HT1080 cells (HT1080 GPX4KO/FSP1OE ). In HT1080 cells, as in many others, knocking out GPX4 induces ferroptosis due to insufficient endogenous FSP1 levels to compensate for GPX4 loss. However, cell survival can be rescued by overexpressing FSP1. Lower right: Upon pharmacological inhibition of FSP1 (iFSP1 treatment), cells undergo ferroptosis as they solely rely on FSP1 function for survival. b , Immunoblot (IB) analysis of ACSL4, FSP1, GPX4, and vinculin in HT1080 parental and HT1080 GPX4KO/FSP1OE cells. c , Dose-dependent toxicity of an FSP1 inhibitor (iFSP1) in HT1080 parental and HT1080 GPX4KO/FSP1OE cell lines. Cell viability was monitored using Alamar blue after 24 h of treatment. Where indicated, cells were treated with the ferroptosis inhibitor Lip-1 (500 nM). d , Schematic representation of the screening strategy used to identify novel factors supporting FSP1 function in the previously-described FSP1-dependent cellular model (see ). HT1080 GPX4KO/FSP1OE cells were transduced with a gRNA library targeting approximately 3000 genes and selected over 7 days in the presence of the ferroptosis inhibitor Lip-1 (500 nM). Subsequently, cells proliferate with or without Lip-1 supplementation for additional 14 days. e, Graphical representation of the results from two independently performed CRISPR screens; plot depicts the score calculated using the MaGeCK package (x-axis) and the –Log false discovery rate (y-axis). Riboflavin kinase (RFK) and stearoyl-CoA desaturase-1 (SCD1) were identified as potentially robust candidates to modulate FSP1 function. f , Immunoblot (IB) analysis of RFK, FSP1, and vinculin in A375 cells transduced with either a non-targeting control (NT) or three different RFK-targeting sgRNAs. g , Dose-dependent toxicity of RSL3 and ML210 in A375 cells transduced with either a non-targeting control (NT) or three different RFK-targeting sgRNAs. Cell viability was monitored after 72 h of treatment.

    Article Snippet: Human cancer cell lines HT1080, A375, MDA-MB-231, MDA-MB-436, A549 and H460 were purchased from ATCC.

    Techniques: Activity Assay, Inhibition, Western Blot, Transduction, CRISPR, Control

    a , Volcano plot of quantified proteins showing their change in A375 parental cells cultured in riboflavin-deficient medium for 96 h. Proteins are plotted based on their fold change (FC: riboflavin deficient/normal). b , Immunoblot (IB) analysis of FSP1, GPX4, and vinculin in HT1080, A375, MDA-MB-231, and A549 parental cell lines after 96 h of growth in riboflavin-deficient medium or medium supplemented with 1 µM riboflavin. c , Lipid peroxidation evaluated by C11-BODIPY 581/591 staining of A375 parental cell line cultured for 72 h in riboflavin-deficient medium or medium supplemented with 1 µM riboflavin and after treatment with DMSO, RSL3 (200 nM), or RSL3 (200 nM) + Lip-1 (500 nM) for 6 h. d , Dose-dependent toxicity of RSL3 in the absence or presence of an FSP1 inhibitor (iFSP1 3 µM) in HT1080, A375, MDA-MB-231, and A549 parental cell lines pre-cultured in riboflavin-deficient medium or medium supplemented with 1 µM riboflavin for 48 h. Cell viability was monitored using Alamar blue after 96 h of treatment. e , Dose-dependent toxicity of RSL3 in the absence or presence of an FSP1 inhibitor (iFSP1 3 µM) in A375 and MDA-MB-231 cells transduced with either a non-targeting control (NT) or an FSP1-targeting sgRNAs pre-cultured in riboflavin-deficient medium or medium supplemented with 1 µM riboflavin for 48 h. Cell viability was monitored after 96 h of treatment. f , Immunoblot (IB) analysis of ACSL4, FSP1, NQO1, and vinculin in A375 and MDA-MB-231 cells transduced with either a non-targeting control (NT) or an FSP1-targeting sgRNAs cultured in riboflavin-deficient medium or medium supplemented with 1 µM riboflavin for 96 h. g , Epilipidomics analysis of A375 parental cells pre-cultured in riboflavin-deficient medium or medium supplemented with 1 µM riboflavin for 72 h after treatment with DMSO, RSL3 (200 nM), or RSL3 (200 nM) + Lip-1 (500 nM) for 6 h.

    Journal: bioRxiv

    Article Title: Riboflavin metabolism shapes FSP1-driven ferroptosis resistance

    doi: 10.1101/2025.08.05.668651

    Figure Lengend Snippet: a , Volcano plot of quantified proteins showing their change in A375 parental cells cultured in riboflavin-deficient medium for 96 h. Proteins are plotted based on their fold change (FC: riboflavin deficient/normal). b , Immunoblot (IB) analysis of FSP1, GPX4, and vinculin in HT1080, A375, MDA-MB-231, and A549 parental cell lines after 96 h of growth in riboflavin-deficient medium or medium supplemented with 1 µM riboflavin. c , Lipid peroxidation evaluated by C11-BODIPY 581/591 staining of A375 parental cell line cultured for 72 h in riboflavin-deficient medium or medium supplemented with 1 µM riboflavin and after treatment with DMSO, RSL3 (200 nM), or RSL3 (200 nM) + Lip-1 (500 nM) for 6 h. d , Dose-dependent toxicity of RSL3 in the absence or presence of an FSP1 inhibitor (iFSP1 3 µM) in HT1080, A375, MDA-MB-231, and A549 parental cell lines pre-cultured in riboflavin-deficient medium or medium supplemented with 1 µM riboflavin for 48 h. Cell viability was monitored using Alamar blue after 96 h of treatment. e , Dose-dependent toxicity of RSL3 in the absence or presence of an FSP1 inhibitor (iFSP1 3 µM) in A375 and MDA-MB-231 cells transduced with either a non-targeting control (NT) or an FSP1-targeting sgRNAs pre-cultured in riboflavin-deficient medium or medium supplemented with 1 µM riboflavin for 48 h. Cell viability was monitored after 96 h of treatment. f , Immunoblot (IB) analysis of ACSL4, FSP1, NQO1, and vinculin in A375 and MDA-MB-231 cells transduced with either a non-targeting control (NT) or an FSP1-targeting sgRNAs cultured in riboflavin-deficient medium or medium supplemented with 1 µM riboflavin for 96 h. g , Epilipidomics analysis of A375 parental cells pre-cultured in riboflavin-deficient medium or medium supplemented with 1 µM riboflavin for 72 h after treatment with DMSO, RSL3 (200 nM), or RSL3 (200 nM) + Lip-1 (500 nM) for 6 h.

    Article Snippet: Human cancer cell lines HT1080, A375, MDA-MB-231, MDA-MB-436, A549 and H460 were purchased from ATCC.

    Techniques: Cell Culture, Western Blot, Staining, Transduction, Control

    a , Immunoblot (IB) analysis of FSP1, GPX4 and vinculin in HT1080, A375, MDA-MB-231 and 549 parental cell lines after 24, 48 and 144 h of growth in riboflavin-deficient medium or supplemented with 1 µM of riboflavin. b , Volcano plots of quantified proteins showing their change in A375 parental cells cultured in riboflavin-deficient medium for 24, 48 and 144 h. Proteins are plotted based on their fold change (FC: riboflavin deficient/normal). c , Heatmaps of quantified proteins showing their change in A375 parental cells cultured in riboflavin-deficient medium for 24, 48, 96 and 144 h (FC: riboflavin deficient/normal). d , Volcano plot of quantified flavoproteins showing their change in A375 parental cells cultured in riboflavin-deficient medium for 96 h (FC: riboflavin deficient/normal). e , Heatmap of quantified flavoproteins showing their change in A375 parental cells cultured in riboflavin-deficient medium for 96 h (FC: riboflavin deficient/normal). f , Lipid peroxidation evaluated by C11-BODIPY 581/591 staining of A375 parental cell line cultured for 72 h in riboflavin-deficient medium or supplemented with 1 µM of riboflavin and after treatment with DMSO, RSL3 (200 nM) or RSL3 (200 nM) + Lip-1 (500 nM) for 6 h. g , Dose-dependent toxicity of RSL3 in the presence of Lip-1 (500 nM) and iFSP1 (3 µM, when indicated) in HT1080, A375, MDA-MB-231 and A549 parental cell lines cultured in riboflavin-deficient medium or supplemented with 1 µM of riboflavin for 48 h. Cell viability was monitored using Alamar blue after 96 h of treatment. h , Absorbance at 517 nm corresponding to the radical initiator 2,2-diphenyl-1-picrylhydrazyl (DPPH) co-incubated with ferrostatin-1 (Fer-1), riboflavin (RbF) or roseoflavin (RoF) (n = 3). Data plotted are mean ± SD. Statistical significance was determined by one-way ANOVA followed by Dunnett’s multiple comparison test.

    Journal: bioRxiv

    Article Title: Riboflavin metabolism shapes FSP1-driven ferroptosis resistance

    doi: 10.1101/2025.08.05.668651

    Figure Lengend Snippet: a , Immunoblot (IB) analysis of FSP1, GPX4 and vinculin in HT1080, A375, MDA-MB-231 and 549 parental cell lines after 24, 48 and 144 h of growth in riboflavin-deficient medium or supplemented with 1 µM of riboflavin. b , Volcano plots of quantified proteins showing their change in A375 parental cells cultured in riboflavin-deficient medium for 24, 48 and 144 h. Proteins are plotted based on their fold change (FC: riboflavin deficient/normal). c , Heatmaps of quantified proteins showing their change in A375 parental cells cultured in riboflavin-deficient medium for 24, 48, 96 and 144 h (FC: riboflavin deficient/normal). d , Volcano plot of quantified flavoproteins showing their change in A375 parental cells cultured in riboflavin-deficient medium for 96 h (FC: riboflavin deficient/normal). e , Heatmap of quantified flavoproteins showing their change in A375 parental cells cultured in riboflavin-deficient medium for 96 h (FC: riboflavin deficient/normal). f , Lipid peroxidation evaluated by C11-BODIPY 581/591 staining of A375 parental cell line cultured for 72 h in riboflavin-deficient medium or supplemented with 1 µM of riboflavin and after treatment with DMSO, RSL3 (200 nM) or RSL3 (200 nM) + Lip-1 (500 nM) for 6 h. g , Dose-dependent toxicity of RSL3 in the presence of Lip-1 (500 nM) and iFSP1 (3 µM, when indicated) in HT1080, A375, MDA-MB-231 and A549 parental cell lines cultured in riboflavin-deficient medium or supplemented with 1 µM of riboflavin for 48 h. Cell viability was monitored using Alamar blue after 96 h of treatment. h , Absorbance at 517 nm corresponding to the radical initiator 2,2-diphenyl-1-picrylhydrazyl (DPPH) co-incubated with ferrostatin-1 (Fer-1), riboflavin (RbF) or roseoflavin (RoF) (n = 3). Data plotted are mean ± SD. Statistical significance was determined by one-way ANOVA followed by Dunnett’s multiple comparison test.

    Article Snippet: Human cancer cell lines HT1080, A375, MDA-MB-231, MDA-MB-436, A549 and H460 were purchased from ATCC.

    Techniques: Western Blot, Cell Culture, Staining, Incubation, Comparison

    a , Schematic representation of the metabolism of riboflavin (RbF) and its analog roseoflavin (RoF) by riboflavin kinase (encoded by RFK ) and FAD synthase (encoded by FLAD1 ). b , Dose-dependent toxicity of roseoflavin (RoF) and iFSP1 in the absence or presence of Lip-1 (500 nM) in HT1080 GPX4KO/FSP1OE . Cell viability was monitored using Alamar blue after 48 h of treatment. Cells were cultured in low-riboflavin medium (20 nM). c , Dose-dependent toxicity of the GPX4 inhibitor ML210 in A375 cells transduced with either a non-targeting control (NT) or a FSP1-targeting sgRNAs (FSP1 KO ) that were pre-treated with roseoflavin (RoF, 1, 3, and 10 nM) for 48 h. Cell viability was monitored after 48 h of ML210 treatment. Cells were cultured in low-riboflavin medium (20 nM). d , Immunoblot analysis (IB) of FSP1, NQO1, ACSL4, GPX4, and vinculin treated with roseoflavin (RoF 0, 20, 100, and 1000 nM) for 96 h in the absence or presence of riboflavin (RbF 20 nM). e , Dose-dependent toxicity of the GPX4 inhibitor ML210 in HT1080, MDA-MB-436, PC-9, and H460 parental cell lines pre-treated with roseoflavin (RoF, 1, 3, and 10 nM) for 48 h. Cell viability was monitored after 48 h of ML210 treatment. f , Immunoblot (IB) analysis of FSP1, NQO1, and vinculin in HT1080, MDA-MB-436, PC9, and H460 parental cell lines treated with roseoflavin (RoF, 20 nM) for 48 h in the absence or presence of riboflavin (RbF 20 nM). g , Riboflavin metabolism supports FSP1 function and promotes ferroptosis resistance. This is therefore a process that riboflavin analogs, such as roseoflavin can modulate.

    Journal: bioRxiv

    Article Title: Riboflavin metabolism shapes FSP1-driven ferroptosis resistance

    doi: 10.1101/2025.08.05.668651

    Figure Lengend Snippet: a , Schematic representation of the metabolism of riboflavin (RbF) and its analog roseoflavin (RoF) by riboflavin kinase (encoded by RFK ) and FAD synthase (encoded by FLAD1 ). b , Dose-dependent toxicity of roseoflavin (RoF) and iFSP1 in the absence or presence of Lip-1 (500 nM) in HT1080 GPX4KO/FSP1OE . Cell viability was monitored using Alamar blue after 48 h of treatment. Cells were cultured in low-riboflavin medium (20 nM). c , Dose-dependent toxicity of the GPX4 inhibitor ML210 in A375 cells transduced with either a non-targeting control (NT) or a FSP1-targeting sgRNAs (FSP1 KO ) that were pre-treated with roseoflavin (RoF, 1, 3, and 10 nM) for 48 h. Cell viability was monitored after 48 h of ML210 treatment. Cells were cultured in low-riboflavin medium (20 nM). d , Immunoblot analysis (IB) of FSP1, NQO1, ACSL4, GPX4, and vinculin treated with roseoflavin (RoF 0, 20, 100, and 1000 nM) for 96 h in the absence or presence of riboflavin (RbF 20 nM). e , Dose-dependent toxicity of the GPX4 inhibitor ML210 in HT1080, MDA-MB-436, PC-9, and H460 parental cell lines pre-treated with roseoflavin (RoF, 1, 3, and 10 nM) for 48 h. Cell viability was monitored after 48 h of ML210 treatment. f , Immunoblot (IB) analysis of FSP1, NQO1, and vinculin in HT1080, MDA-MB-436, PC9, and H460 parental cell lines treated with roseoflavin (RoF, 20 nM) for 48 h in the absence or presence of riboflavin (RbF 20 nM). g , Riboflavin metabolism supports FSP1 function and promotes ferroptosis resistance. This is therefore a process that riboflavin analogs, such as roseoflavin can modulate.

    Article Snippet: Human cancer cell lines HT1080, A375, MDA-MB-231, MDA-MB-436, A549 and H460 were purchased from ATCC.

    Techniques: Cell Culture, Transduction, Control, Western Blot