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sw1990 cells  (ATCC)


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    ATCC sw1990 cells
    Sw1990 Cells, 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
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    Average 97 stars, based on 1327 article reviews
    sw1990 cells - by Bioz Stars, 2026-04
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    ATCC sw1990 cells
    Sw1990 Cells, 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
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    ATCC cell lines sw1990 atcc crl 2172 tm bxpc3 atcc crl 1687 tm thp 1 atcc tib 202 tm bxpc3 r gem resistant
    Cell Lines Sw1990 Atcc Crl 2172 Tm Bxpc3 Atcc Crl 1687 Tm Thp 1 Atcc Tib 202 Tm Bxpc3 R Gem Resistant, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC sw1990 cell lines
    Sw1990 Cell Lines, 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
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    ATCC pancreatic carcinoma cell lines sw1990
    Transwell assay was used for assessment of anti-invasive potential of the Ph-triazole against <t>SW1990</t> and PANC-1 cells in vitro after incubation with 0.5, 8, and 32 µM concentrations. Quantification of the invaded cells was performed, and pictures were taken at x100 magnification. ** p < 0.01 and * p < 0.05 relative to control cells.
    Pancreatic Carcinoma 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
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    ATCC pancreatic cancer cell lines sw1990
    Transwell assay was used for assessment of anti-invasive potential of the Ph-triazole against <t>SW1990</t> and PANC-1 cells in vitro after incubation with 0.5, 8, and 32 µM concentrations. Quantification of the invaded cells was performed, and pictures were taken at x100 magnification. ** p < 0.01 and * p < 0.05 relative to control cells.
    Pancreatic Cancer 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/pancreatic cancer cell lines sw1990/product/ATCC
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    ATCC sw1990 parental cells
    A – D <t>SW1990</t> cells stably engineered for doxycycline-inducible regulatable sh236 KRAS-specific shRNA expression and CMV-driven constitutive expression of the various flag-tagged KRAS G12D alleles without (FK G12D ) or with discrete mutations within the back-pocket (FK G12D/L23E or FK G12D / V45D or FK G12D/V45D/L23E ) were treated for 72 h with doxycycline, lyzed and cell extracts further analyzed either by straight western-blot for the indicated read-outs ( A and C ), or by GST-cRaf-RBD pull-down to quantify GTP-loaded exogenously expressed KRAS binding ( B , upper panel), or by anti-flag co-immuno-precipitation for endogenous proteins ( D , upper panel). For ( B , D ), Input (lower panels) refer to straight western blots to assess expression levels across the conditions tested. E , F SW1990 cells stably engineered for doxycycline-inducible regulatable non targeting shNT control or sh236 KRAS-specific shRNA expression and Ubc-driven constitutive expression of the various flag-tagged KRAS G12D and KRAS G12D/V45D alleles were treated with doxycycline for either 14 days in a colony formation assay (left panel), or for 3 days only at which stage cells were lyzed and cell extracts analyzed by western-blot for the mentioned read-outs. Con.: control cells engineered from CMV-driven empty vector; SE: Short Exposure; LE: Long Exposure; a: endogenous KRAS G12D ; b: flag-tagged exogenously expressed KRAS. For ( A – F ), a minimum of three repeats has been performed with similar results; Source Data are provided as a Source Data file.
    Sw1990 Parental Cells, 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
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    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
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    ATCC sw1990 cells atcc cat
    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.
    Sw1990 Cells Atcc Cat, 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
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    Transwell assay was used for assessment of anti-invasive potential of the Ph-triazole against SW1990 and PANC-1 cells in vitro after incubation with 0.5, 8, and 32 µM concentrations. Quantification of the invaded cells was performed, and pictures were taken at x100 magnification. ** p < 0.01 and * p < 0.05 relative to control cells.

    Journal: PLOS One

    Article Title: Ph-triazole as a therapeutic agent for pancreatic cancer: Synthesis, in silico, and in vitro evaluation

    doi: 10.1371/journal.pone.0334618

    Figure Lengend Snippet: Transwell assay was used for assessment of anti-invasive potential of the Ph-triazole against SW1990 and PANC-1 cells in vitro after incubation with 0.5, 8, and 32 µM concentrations. Quantification of the invaded cells was performed, and pictures were taken at x100 magnification. ** p < 0.01 and * p < 0.05 relative to control cells.

    Article Snippet: The pancreatic carcinoma cell lines SW1990 and PANC-1 as well as the normal pancreatic duct epithelial cell line (HPDE6-C7) were provided by the American Type Culture Collection (ATCC).

    Techniques: Transwell Assay, In Vitro, Incubation, Control

    The cells were incubated with 0.5, 8, and 32 µM concentration of Ph-triazole for 72 h in an incubator at 37 °C. Western blotting was performed to assess the expression P53 in SW1990 and PANC-1 cells. ** p < 0.01 and * p < 0.05 relative to control cells.

    Journal: PLOS One

    Article Title: Ph-triazole as a therapeutic agent for pancreatic cancer: Synthesis, in silico, and in vitro evaluation

    doi: 10.1371/journal.pone.0334618

    Figure Lengend Snippet: The cells were incubated with 0.5, 8, and 32 µM concentration of Ph-triazole for 72 h in an incubator at 37 °C. Western blotting was performed to assess the expression P53 in SW1990 and PANC-1 cells. ** p < 0.01 and * p < 0.05 relative to control cells.

    Article Snippet: The pancreatic carcinoma cell lines SW1990 and PANC-1 as well as the normal pancreatic duct epithelial cell line (HPDE6-C7) were provided by the American Type Culture Collection (ATCC).

    Techniques: Incubation, Concentration Assay, Western Blot, Expressing, Control

    A – D SW1990 cells stably engineered for doxycycline-inducible regulatable sh236 KRAS-specific shRNA expression and CMV-driven constitutive expression of the various flag-tagged KRAS G12D alleles without (FK G12D ) or with discrete mutations within the back-pocket (FK G12D/L23E or FK G12D / V45D or FK G12D/V45D/L23E ) were treated for 72 h with doxycycline, lyzed and cell extracts further analyzed either by straight western-blot for the indicated read-outs ( A and C ), or by GST-cRaf-RBD pull-down to quantify GTP-loaded exogenously expressed KRAS binding ( B , upper panel), or by anti-flag co-immuno-precipitation for endogenous proteins ( D , upper panel). For ( B , D ), Input (lower panels) refer to straight western blots to assess expression levels across the conditions tested. E , F SW1990 cells stably engineered for doxycycline-inducible regulatable non targeting shNT control or sh236 KRAS-specific shRNA expression and Ubc-driven constitutive expression of the various flag-tagged KRAS G12D and KRAS G12D/V45D alleles were treated with doxycycline for either 14 days in a colony formation assay (left panel), or for 3 days only at which stage cells were lyzed and cell extracts analyzed by western-blot for the mentioned read-outs. Con.: control cells engineered from CMV-driven empty vector; SE: Short Exposure; LE: Long Exposure; a: endogenous KRAS G12D ; b: flag-tagged exogenously expressed KRAS. For ( A – F ), a minimum of three repeats has been performed with similar results; Source Data are provided as a Source Data file.

    Journal: Nature Communications

    Article Title: Identification and characterization of binders to a cryptic and functional pocket in KRAS

    doi: 10.1038/s41467-025-65844-3

    Figure Lengend Snippet: A – D SW1990 cells stably engineered for doxycycline-inducible regulatable sh236 KRAS-specific shRNA expression and CMV-driven constitutive expression of the various flag-tagged KRAS G12D alleles without (FK G12D ) or with discrete mutations within the back-pocket (FK G12D/L23E or FK G12D / V45D or FK G12D/V45D/L23E ) were treated for 72 h with doxycycline, lyzed and cell extracts further analyzed either by straight western-blot for the indicated read-outs ( A and C ), or by GST-cRaf-RBD pull-down to quantify GTP-loaded exogenously expressed KRAS binding ( B , upper panel), or by anti-flag co-immuno-precipitation for endogenous proteins ( D , upper panel). For ( B , D ), Input (lower panels) refer to straight western blots to assess expression levels across the conditions tested. E , F SW1990 cells stably engineered for doxycycline-inducible regulatable non targeting shNT control or sh236 KRAS-specific shRNA expression and Ubc-driven constitutive expression of the various flag-tagged KRAS G12D and KRAS G12D/V45D alleles were treated with doxycycline for either 14 days in a colony formation assay (left panel), or for 3 days only at which stage cells were lyzed and cell extracts analyzed by western-blot for the mentioned read-outs. Con.: control cells engineered from CMV-driven empty vector; SE: Short Exposure; LE: Long Exposure; a: endogenous KRAS G12D ; b: flag-tagged exogenously expressed KRAS. For ( A – F ), a minimum of three repeats has been performed with similar results; Source Data are provided as a Source Data file.

    Article Snippet: SW1990 (ATCC #CRL-2172) and all the engineered lines from the SW1990 parental cells were cultured in RPMI 1640 media with Glutamax, supplemented with 10% FBS, 1 mM Sodium pyruvate, 10 mM HEPES at 37 °C with 5% CO 2 .

    Techniques: Stable Transfection, shRNA, Expressing, Western Blot, Binding Assay, Immunoprecipitation, Control, Colony Assay, Plasmid Preparation

    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