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ATCC human pdac cell line sw1990
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ATCC sw1990 cells
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Procell Inc pancreatic cancer cells sw1990
G6PD Inhibitor RRx-001 Activates Disulfide-Mediated Cell Death in <t>SW1990</t> Cells. A Molecular docking and optimization of RRx-001 with G6PD. B CCK-8 assay to detect the proliferation capacity of SW1990 cells. C-E Flow cytometry analysis of SW1990 cell death rates. F WST-8 colorimetric assay to measure NADPH levels in SW1990 cells. G Fluorescence microplate assay to determine cystine uptake capacity in SW1990 cells. H Representative immunofluorescence images of F-actin (phalloidin staining) and nuclei (DAPI) in SW1990 cells treated with RRx-001 or vehicle control. I Quantification of immunofluorescence staining. * p < 0.05, ** p < 0.01, *** p < 0.001
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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
G6PD Inhibitor RRx-001 Activates Disulfide-Mediated Cell Death in <t>SW1990</t> Cells. A Molecular docking and optimization of RRx-001 with G6PD. B CCK-8 assay to detect the proliferation capacity of SW1990 cells. C-E Flow cytometry analysis of SW1990 cell death rates. F WST-8 colorimetric assay to measure NADPH levels in SW1990 cells. G Fluorescence microplate assay to determine cystine uptake capacity in SW1990 cells. H Representative immunofluorescence images of F-actin (phalloidin staining) and nuclei (DAPI) in SW1990 cells treated with RRx-001 or vehicle control. I Quantification of immunofluorescence staining. * p < 0.05, ** p < 0.01, *** p < 0.001
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
G6PD Inhibitor RRx-001 Activates Disulfide-Mediated Cell Death in <t>SW1990</t> Cells. A Molecular docking and optimization of RRx-001 with G6PD. B CCK-8 assay to detect the proliferation capacity of SW1990 cells. C-E Flow cytometry analysis of SW1990 cell death rates. F WST-8 colorimetric assay to measure NADPH levels in SW1990 cells. G Fluorescence microplate assay to determine cystine uptake capacity in SW1990 cells. H Representative immunofluorescence images of F-actin (phalloidin staining) and nuclei (DAPI) in SW1990 cells treated with RRx-001 or vehicle control. I Quantification of immunofluorescence staining. * p < 0.05, ** p < 0.01, *** p < 0.001
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/product/sw1990+cells/SW+1990/pm41349909-54-34-41
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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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G6PD Inhibitor RRx-001 Activates Disulfide-Mediated Cell Death in SW1990 Cells. A Molecular docking and optimization of RRx-001 with G6PD. B CCK-8 assay to detect the proliferation capacity of SW1990 cells. C-E Flow cytometry analysis of SW1990 cell death rates. F WST-8 colorimetric assay to measure NADPH levels in SW1990 cells. G Fluorescence microplate assay to determine cystine uptake capacity in SW1990 cells. H Representative immunofluorescence images of F-actin (phalloidin staining) and nuclei (DAPI) in SW1990 cells treated with RRx-001 or vehicle control. I Quantification of immunofluorescence staining. * p < 0.05, ** p < 0.01, *** p < 0.001

Journal: Discover Oncology

Article Title: Identification of the disulfidptosis-related gene G6PD as a potential biomarker and therapeutic target in pancreatic ductal adenocarcinoma by integrative bioinformatics analysis and experimental validation

doi: 10.1007/s12672-026-04753-3

Figure Lengend Snippet: G6PD Inhibitor RRx-001 Activates Disulfide-Mediated Cell Death in SW1990 Cells. A Molecular docking and optimization of RRx-001 with G6PD. B CCK-8 assay to detect the proliferation capacity of SW1990 cells. C-E Flow cytometry analysis of SW1990 cell death rates. F WST-8 colorimetric assay to measure NADPH levels in SW1990 cells. G Fluorescence microplate assay to determine cystine uptake capacity in SW1990 cells. H Representative immunofluorescence images of F-actin (phalloidin staining) and nuclei (DAPI) in SW1990 cells treated with RRx-001 or vehicle control. I Quantification of immunofluorescence staining. * p < 0.05, ** p < 0.01, *** p < 0.001

Article Snippet: Human pancreatic ductal epithelial cells (HPDE-C7) and pancreatic cancer cells (SW1990) were purchased from Procell Life Science & Technology Co., Ltd. (Wuhan, China).

Techniques: CCK-8 Assay, Flow Cytometry, Colorimetric Assay, Fluorescence, Immunofluorescence, Staining, Control

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