Review



human tumor cell lines sw1990  (ATCC)


Bioz Verified Symbol ATCC is a verified supplier
Bioz Manufacturer Symbol ATCC manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 97
      Buy from Supplier

    Structured Review

    ATCC human tumor cell lines sw1990
    Antibiotics screening identifies ciprofloxacin (CFX) synergies with RSL3 to inhibit PDAC cell viability. A, PANC1 cells were treated with 50 antibiotics (20, 30, 40, and 50 μg/ml) in combination with RSL3 (0.25, 0.5, 0.75, and 1 μM) at four concentration gradients for 24 h. Cell viability was measured by CCK-8 assay. Synergy score for drug combinations quantified by zero interaction potency (ZIP) model in SynergyFinder web application (version 3.0). Synergy score less than −10 means antagonistic, from −10 to 10 means additive, and larger than 10 means synergistic. B, heatmap representing ZIP synergy score of the 50 antibiotics in combination with RSL3 for treatment of PANC1 cells. Data were representative of independent experiments. C, cell viability curves of PANC1, <t>SW1990,</t> HeLa, and OVCAR-3 cells treated with different concentrations of CFX in combination with RSL3 for 24 h. D, ZIP synergy scores of CFX in combination with RSL3 in PANC1, SW1990, HeLa, and OVCAR-3 cells. E, clone formation image of PANC1, SW1990, and HeLa cells untreated (Ctrl group) or treated with RSL3 (0.5 μM) in the presence or absence of CFX (50 μg/ml) for 24 h, and cell clone formation was detected after 2 weeks. Data are presented as the mean ± SD from at least three independent experiments. p Values were calculated using two-way ANOVA ( C ) or one-way ANOVA ( E ). CCK-8, Cell Counting Kit-8; PDAC, pancreatic ductal adenocarcinoma.
    Human Tumor Cell Lines Sw1990, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1327 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human tumor cell lines sw1990/product/ATCC
    Average 97 stars, based on 1327 article reviews
    human tumor cell lines sw1990 - by Bioz Stars, 2026-04
    97/100 stars

    Images

    1) Product Images from "Ciprofloxacin enhances RSL3-induced ferroptosis by promoting mitochondrial Zn 2+ accumulation via the STING1–CAV2 pathway"

    Article Title: Ciprofloxacin enhances RSL3-induced ferroptosis by promoting mitochondrial Zn 2+ accumulation via the STING1–CAV2 pathway

    Journal: The Journal of Biological Chemistry

    doi: 10.1016/j.jbc.2025.110653

    Antibiotics screening identifies ciprofloxacin (CFX) synergies with RSL3 to inhibit PDAC cell viability. A, PANC1 cells were treated with 50 antibiotics (20, 30, 40, and 50 μg/ml) in combination with RSL3 (0.25, 0.5, 0.75, and 1 μM) at four concentration gradients for 24 h. Cell viability was measured by CCK-8 assay. Synergy score for drug combinations quantified by zero interaction potency (ZIP) model in SynergyFinder web application (version 3.0). Synergy score less than −10 means antagonistic, from −10 to 10 means additive, and larger than 10 means synergistic. B, heatmap representing ZIP synergy score of the 50 antibiotics in combination with RSL3 for treatment of PANC1 cells. Data were representative of independent experiments. C, cell viability curves of PANC1, SW1990, HeLa, and OVCAR-3 cells treated with different concentrations of CFX in combination with RSL3 for 24 h. D, ZIP synergy scores of CFX in combination with RSL3 in PANC1, SW1990, HeLa, and OVCAR-3 cells. E, clone formation image of PANC1, SW1990, and HeLa cells untreated (Ctrl group) or treated with RSL3 (0.5 μM) in the presence or absence of CFX (50 μg/ml) for 24 h, and cell clone formation was detected after 2 weeks. Data are presented as the mean ± SD from at least three independent experiments. p Values were calculated using two-way ANOVA ( C ) or one-way ANOVA ( E ). CCK-8, Cell Counting Kit-8; PDAC, pancreatic ductal adenocarcinoma.
    Figure Legend Snippet: Antibiotics screening identifies ciprofloxacin (CFX) synergies with RSL3 to inhibit PDAC cell viability. A, PANC1 cells were treated with 50 antibiotics (20, 30, 40, and 50 μg/ml) in combination with RSL3 (0.25, 0.5, 0.75, and 1 μM) at four concentration gradients for 24 h. Cell viability was measured by CCK-8 assay. Synergy score for drug combinations quantified by zero interaction potency (ZIP) model in SynergyFinder web application (version 3.0). Synergy score less than −10 means antagonistic, from −10 to 10 means additive, and larger than 10 means synergistic. B, heatmap representing ZIP synergy score of the 50 antibiotics in combination with RSL3 for treatment of PANC1 cells. Data were representative of independent experiments. C, cell viability curves of PANC1, SW1990, HeLa, and OVCAR-3 cells treated with different concentrations of CFX in combination with RSL3 for 24 h. D, ZIP synergy scores of CFX in combination with RSL3 in PANC1, SW1990, HeLa, and OVCAR-3 cells. E, clone formation image of PANC1, SW1990, and HeLa cells untreated (Ctrl group) or treated with RSL3 (0.5 μM) in the presence or absence of CFX (50 μg/ml) for 24 h, and cell clone formation was detected after 2 weeks. Data are presented as the mean ± SD from at least three independent experiments. p Values were calculated using two-way ANOVA ( C ) or one-way ANOVA ( E ). CCK-8, Cell Counting Kit-8; PDAC, pancreatic ductal adenocarcinoma.

    Techniques Used: Concentration Assay, CCK-8 Assay, Cell Counting

    Ciprofloxacin (CFX) amplifies RSL3-driven ferroptosis. A, cell viability of PANC1, SW1990, and HeLa cells following treatment with different concentrations of CFX for 24 h. B, cell viability of PANC1, SW1990, and HeLa cells treated with RSL3 in the presence or absence of CFX (50 μg/ml) and liproxstatin-1 (Lip-1, 1 μM) for 24 h. C, representative Hoechst 33342 and propidium iodide (PI) staining images of PANC1, SW1990, and HeLa cells treated with RSL3 (1 μM) in the presence or absence of CFX (50 μg/ml) and Lip-1 (1 μM) for 24 h. Scale bar represents 200 μm. Quantification of PI-positive cells is shown. D, lipid reactive oxygen species (ROS) of PANC1 and SW1990 cells treated with RSL3 (1 μM) in the presence or absence of CFX (50 μg/ml) and ferrostatin-1 (Fer-1, 1 μM) for 12 h. E, malondialdehyde (MDA) of PANC1 and SW1990 cells treated with RSL3 (1 μM) in the presence or absence of CFX (50 μg/ml) for 12 h. F, fluorescence imaging of Phen Green SK (Fe 2+ indicator) in PANC1 and HeLa cells treated with RSL3 (1 μM) in the presence or absence of CFX (50 μg/ml) for 12 h. Scale bar represents 200 μm. The relative fluorescence intensity is shown. G, GSH level of PANC1 cells treated with RSL3 (1 μM) in the presence or absence of CFX (50 μg/ml) for 12 h. H, cell viability of PANC1 and HeLa cells treated with CFX (50 μg/ml) in the presence or absence of RSL3 (1 μM), staurosporine (STS, 1 μM), and TSZ (tumor necrosis factor-α, SM-164, and Z-VAD-FMK) for 24 h. Cell viability of PANC1 and HeLa cells treated with STS (1 μM) and TSZ (TNF-α, SM-164, and Z-VAD-FMK) in the presence or absence of the corresponding inhibitors (Z-VAD-FMK, 20 μM; necrosulfonamide/NSA, 2 μM) for 24 h. Data are presented as the mean ± SD from at least three independent experiments. p Values were calculated using two-way ANOVA ( B ) or one-way ANOVA ( C – H ). ns means no significance.
    Figure Legend Snippet: Ciprofloxacin (CFX) amplifies RSL3-driven ferroptosis. A, cell viability of PANC1, SW1990, and HeLa cells following treatment with different concentrations of CFX for 24 h. B, cell viability of PANC1, SW1990, and HeLa cells treated with RSL3 in the presence or absence of CFX (50 μg/ml) and liproxstatin-1 (Lip-1, 1 μM) for 24 h. C, representative Hoechst 33342 and propidium iodide (PI) staining images of PANC1, SW1990, and HeLa cells treated with RSL3 (1 μM) in the presence or absence of CFX (50 μg/ml) and Lip-1 (1 μM) for 24 h. Scale bar represents 200 μm. Quantification of PI-positive cells is shown. D, lipid reactive oxygen species (ROS) of PANC1 and SW1990 cells treated with RSL3 (1 μM) in the presence or absence of CFX (50 μg/ml) and ferrostatin-1 (Fer-1, 1 μM) for 12 h. E, malondialdehyde (MDA) of PANC1 and SW1990 cells treated with RSL3 (1 μM) in the presence or absence of CFX (50 μg/ml) for 12 h. F, fluorescence imaging of Phen Green SK (Fe 2+ indicator) in PANC1 and HeLa cells treated with RSL3 (1 μM) in the presence or absence of CFX (50 μg/ml) for 12 h. Scale bar represents 200 μm. The relative fluorescence intensity is shown. G, GSH level of PANC1 cells treated with RSL3 (1 μM) in the presence or absence of CFX (50 μg/ml) for 12 h. H, cell viability of PANC1 and HeLa cells treated with CFX (50 μg/ml) in the presence or absence of RSL3 (1 μM), staurosporine (STS, 1 μM), and TSZ (tumor necrosis factor-α, SM-164, and Z-VAD-FMK) for 24 h. Cell viability of PANC1 and HeLa cells treated with STS (1 μM) and TSZ (TNF-α, SM-164, and Z-VAD-FMK) in the presence or absence of the corresponding inhibitors (Z-VAD-FMK, 20 μM; necrosulfonamide/NSA, 2 μM) for 24 h. Data are presented as the mean ± SD from at least three independent experiments. p Values were calculated using two-way ANOVA ( B ) or one-way ANOVA ( C – H ). ns means no significance.

    Techniques Used: Staining, Fluorescence, Imaging



    Similar Products

    human tumor cell lines sw1990  (ATCC)
    97
    ATCC human tumor cell lines sw1990
    Antibiotics screening identifies ciprofloxacin (CFX) synergies with RSL3 to inhibit PDAC cell viability. A, PANC1 cells were treated with 50 antibiotics (20, 30, 40, and 50 μg/ml) in combination with RSL3 (0.25, 0.5, 0.75, and 1 μM) at four concentration gradients for 24 h. Cell viability was measured by CCK-8 assay. Synergy score for drug combinations quantified by zero interaction potency (ZIP) model in SynergyFinder web application (version 3.0). Synergy score less than −10 means antagonistic, from −10 to 10 means additive, and larger than 10 means synergistic. B, heatmap representing ZIP synergy score of the 50 antibiotics in combination with RSL3 for treatment of PANC1 cells. Data were representative of independent experiments. C, cell viability curves of PANC1, <t>SW1990,</t> HeLa, and OVCAR-3 cells treated with different concentrations of CFX in combination with RSL3 for 24 h. D, ZIP synergy scores of CFX in combination with RSL3 in PANC1, SW1990, HeLa, and OVCAR-3 cells. E, clone formation image of PANC1, SW1990, and HeLa cells untreated (Ctrl group) or treated with RSL3 (0.5 μM) in the presence or absence of CFX (50 μg/ml) for 24 h, and cell clone formation was detected after 2 weeks. Data are presented as the mean ± SD from at least three independent experiments. p Values were calculated using two-way ANOVA ( C ) or one-way ANOVA ( E ). CCK-8, Cell Counting Kit-8; PDAC, pancreatic ductal adenocarcinoma.
    Human Tumor Cell Lines Sw1990, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human tumor cell lines sw1990/product/ATCC
    Average 97 stars, based on 1 article reviews
    human tumor cell lines sw1990 - by Bioz Stars, 2026-04
    97/100 stars
    		  Buy from Supplier

    Image Search Results


    Antibiotics screening identifies ciprofloxacin (CFX) synergies with RSL3 to inhibit PDAC cell viability. A, PANC1 cells were treated with 50 antibiotics (20, 30, 40, and 50 μg/ml) in combination with RSL3 (0.25, 0.5, 0.75, and 1 μM) at four concentration gradients for 24 h. Cell viability was measured by CCK-8 assay. Synergy score for drug combinations quantified by zero interaction potency (ZIP) model in SynergyFinder web application (version 3.0). Synergy score less than −10 means antagonistic, from −10 to 10 means additive, and larger than 10 means synergistic. B, heatmap representing ZIP synergy score of the 50 antibiotics in combination with RSL3 for treatment of PANC1 cells. Data were representative of independent experiments. C, cell viability curves of PANC1, SW1990, HeLa, and OVCAR-3 cells treated with different concentrations of CFX in combination with RSL3 for 24 h. D, ZIP synergy scores of CFX in combination with RSL3 in PANC1, SW1990, HeLa, and OVCAR-3 cells. E, clone formation image of PANC1, SW1990, and HeLa cells untreated (Ctrl group) or treated with RSL3 (0.5 μM) in the presence or absence of CFX (50 μg/ml) for 24 h, and cell clone formation was detected after 2 weeks. Data are presented as the mean ± SD from at least three independent experiments. p Values were calculated using two-way ANOVA ( C ) or one-way ANOVA ( E ). CCK-8, Cell Counting Kit-8; PDAC, pancreatic ductal adenocarcinoma.

    Journal: The Journal of Biological Chemistry

    Article Title: Ciprofloxacin enhances RSL3-induced ferroptosis by promoting mitochondrial Zn 2+ accumulation via the STING1–CAV2 pathway

    doi: 10.1016/j.jbc.2025.110653

    Figure Lengend Snippet: Antibiotics screening identifies ciprofloxacin (CFX) synergies with RSL3 to inhibit PDAC cell viability. A, PANC1 cells were treated with 50 antibiotics (20, 30, 40, and 50 μg/ml) in combination with RSL3 (0.25, 0.5, 0.75, and 1 μM) at four concentration gradients for 24 h. Cell viability was measured by CCK-8 assay. Synergy score for drug combinations quantified by zero interaction potency (ZIP) model in SynergyFinder web application (version 3.0). Synergy score less than −10 means antagonistic, from −10 to 10 means additive, and larger than 10 means synergistic. B, heatmap representing ZIP synergy score of the 50 antibiotics in combination with RSL3 for treatment of PANC1 cells. Data were representative of independent experiments. C, cell viability curves of PANC1, SW1990, HeLa, and OVCAR-3 cells treated with different concentrations of CFX in combination with RSL3 for 24 h. D, ZIP synergy scores of CFX in combination with RSL3 in PANC1, SW1990, HeLa, and OVCAR-3 cells. E, clone formation image of PANC1, SW1990, and HeLa cells untreated (Ctrl group) or treated with RSL3 (0.5 μM) in the presence or absence of CFX (50 μg/ml) for 24 h, and cell clone formation was detected after 2 weeks. Data are presented as the mean ± SD from at least three independent experiments. p Values were calculated using two-way ANOVA ( C ) or one-way ANOVA ( E ). CCK-8, Cell Counting Kit-8; PDAC, pancreatic ductal adenocarcinoma.

    Article Snippet: Human tumor cell lines SW1990 (CRL-2172), PANC1 (CRL-1469), HeLa (CCL-2), and OVCAR-3 (HTB-161) were procured from the American Type Culture Collection and examined every 3 months to ensure they remained free of mycoplasma contamination.

    Techniques: Concentration Assay, CCK-8 Assay, Cell Counting

    Ciprofloxacin (CFX) amplifies RSL3-driven ferroptosis. A, cell viability of PANC1, SW1990, and HeLa cells following treatment with different concentrations of CFX for 24 h. B, cell viability of PANC1, SW1990, and HeLa cells treated with RSL3 in the presence or absence of CFX (50 μg/ml) and liproxstatin-1 (Lip-1, 1 μM) for 24 h. C, representative Hoechst 33342 and propidium iodide (PI) staining images of PANC1, SW1990, and HeLa cells treated with RSL3 (1 μM) in the presence or absence of CFX (50 μg/ml) and Lip-1 (1 μM) for 24 h. Scale bar represents 200 μm. Quantification of PI-positive cells is shown. D, lipid reactive oxygen species (ROS) of PANC1 and SW1990 cells treated with RSL3 (1 μM) in the presence or absence of CFX (50 μg/ml) and ferrostatin-1 (Fer-1, 1 μM) for 12 h. E, malondialdehyde (MDA) of PANC1 and SW1990 cells treated with RSL3 (1 μM) in the presence or absence of CFX (50 μg/ml) for 12 h. F, fluorescence imaging of Phen Green SK (Fe 2+ indicator) in PANC1 and HeLa cells treated with RSL3 (1 μM) in the presence or absence of CFX (50 μg/ml) for 12 h. Scale bar represents 200 μm. The relative fluorescence intensity is shown. G, GSH level of PANC1 cells treated with RSL3 (1 μM) in the presence or absence of CFX (50 μg/ml) for 12 h. H, cell viability of PANC1 and HeLa cells treated with CFX (50 μg/ml) in the presence or absence of RSL3 (1 μM), staurosporine (STS, 1 μM), and TSZ (tumor necrosis factor-α, SM-164, and Z-VAD-FMK) for 24 h. Cell viability of PANC1 and HeLa cells treated with STS (1 μM) and TSZ (TNF-α, SM-164, and Z-VAD-FMK) in the presence or absence of the corresponding inhibitors (Z-VAD-FMK, 20 μM; necrosulfonamide/NSA, 2 μM) for 24 h. Data are presented as the mean ± SD from at least three independent experiments. p Values were calculated using two-way ANOVA ( B ) or one-way ANOVA ( C – H ). ns means no significance.

    Journal: The Journal of Biological Chemistry

    Article Title: Ciprofloxacin enhances RSL3-induced ferroptosis by promoting mitochondrial Zn 2+ accumulation via the STING1–CAV2 pathway

    doi: 10.1016/j.jbc.2025.110653

    Figure Lengend Snippet: Ciprofloxacin (CFX) amplifies RSL3-driven ferroptosis. A, cell viability of PANC1, SW1990, and HeLa cells following treatment with different concentrations of CFX for 24 h. B, cell viability of PANC1, SW1990, and HeLa cells treated with RSL3 in the presence or absence of CFX (50 μg/ml) and liproxstatin-1 (Lip-1, 1 μM) for 24 h. C, representative Hoechst 33342 and propidium iodide (PI) staining images of PANC1, SW1990, and HeLa cells treated with RSL3 (1 μM) in the presence or absence of CFX (50 μg/ml) and Lip-1 (1 μM) for 24 h. Scale bar represents 200 μm. Quantification of PI-positive cells is shown. D, lipid reactive oxygen species (ROS) of PANC1 and SW1990 cells treated with RSL3 (1 μM) in the presence or absence of CFX (50 μg/ml) and ferrostatin-1 (Fer-1, 1 μM) for 12 h. E, malondialdehyde (MDA) of PANC1 and SW1990 cells treated with RSL3 (1 μM) in the presence or absence of CFX (50 μg/ml) for 12 h. F, fluorescence imaging of Phen Green SK (Fe 2+ indicator) in PANC1 and HeLa cells treated with RSL3 (1 μM) in the presence or absence of CFX (50 μg/ml) for 12 h. Scale bar represents 200 μm. The relative fluorescence intensity is shown. G, GSH level of PANC1 cells treated with RSL3 (1 μM) in the presence or absence of CFX (50 μg/ml) for 12 h. H, cell viability of PANC1 and HeLa cells treated with CFX (50 μg/ml) in the presence or absence of RSL3 (1 μM), staurosporine (STS, 1 μM), and TSZ (tumor necrosis factor-α, SM-164, and Z-VAD-FMK) for 24 h. Cell viability of PANC1 and HeLa cells treated with STS (1 μM) and TSZ (TNF-α, SM-164, and Z-VAD-FMK) in the presence or absence of the corresponding inhibitors (Z-VAD-FMK, 20 μM; necrosulfonamide/NSA, 2 μM) for 24 h. Data are presented as the mean ± SD from at least three independent experiments. p Values were calculated using two-way ANOVA ( B ) or one-way ANOVA ( C – H ). ns means no significance.

    Article Snippet: Human tumor cell lines SW1990 (CRL-2172), PANC1 (CRL-1469), HeLa (CCL-2), and OVCAR-3 (HTB-161) were procured from the American Type Culture Collection and examined every 3 months to ensure they remained free of mycoplasma contamination.

    Techniques: Staining, Fluorescence, Imaging