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human pdac cell lines panc1  (ATCC)


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    ATCC human pdac cell lines panc1
    Human Pdac Cell Lines Panc1, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 8072 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+pdac+cell+lines+panc1/PANC-1/pm40614202-266-1-21
    Average 99 stars, based on 8072 article reviews
    human pdac cell lines panc1 - by Bioz Stars, 2026-09
    99/100 stars

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    Related Articles

    Multiple Displacement Amplification:

    Article Title: The Modulatory Role of MicroRNA-873 in the Progression of KRAS-Driven Cancers.
    Article Snippet: .. The human mammary epithelial cell line MCF10A; breast cancer cell lines MDA-MB-436, MDA-MB-231, MDA-MB-453, BT-20, HCC1937, SKBR3, T47D, and HEK293; normal HPDE cells; and human PDAC cell lines PANC1, BxPC-3, MiaPaCa-2, and Capan-2 were purchased from the American Type Culture Collection (Manassas, VA). .. All breast cancer cells and PANC1 and MiaPaCa-2 cells were cultured in DMEM/F12 (Sigma, St. Louis, MO).



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    MRTX1133 inhibits the growth of <t>PDAC</t> cells in “low”- but not “high”-confluent collagen cultures. A, PDAC cells (1 × 10 5 ) were grown in floating collagen gels (1.2 mg/mL) for 48 hours to generate “low”-confluent cultures. Depiction of “low”-confluent floating collagen cultures. B, PDAC cell lines (2138, 3213, 1245, <t>PANC1)</t> grown in “low”-confluent collagen cultures were treated with MRTX1133 (0.5 µmol/L) for 8 hours, and the effect on ERK1/2 phosphorylation was analyzed by Western blotting. Blots are representative of at least three biological replicates. C, PDAC cell lines grown in “low”-confluent collagen cultures were treated with DMSO or 0.5 µmol/L MRTX1133 for 72 hours. The cells were imaged at baseline and after 1, 2, and 3 days of treatment, and the relative growth was quantified. Error bars, ± SD; n = 3, unpaired t test. **, P < 0.01; ***, P < 0.001. Scale bar, 100 μm. D, PDAC cells (1 × 10 5 ) were grown in floating collagen gels (1.2 mg/mL) for 96 to 120 hours to generate “high-confluent” cultures. Depiction of “high-confluent” floating collagen cultures. E, PDAC cell lines grown in “high-confluent” collagen cultures were treated with MRTX1133 (0.5 µmol/L) for 8 hours, and the effect on ERK1/2 phosphorylation was analyzed by Western blotting. Blots are representative of at least three biological replicates. F, PDAC cell lines grown in “high-confluent” collagen cultures were treated with DMSO or 0.5 µmol/L MRTX1133 for 72 hours. The cells were imaged at baseline and after 1, 2, and 3 days of treatment, and the relative growth was quantified. Error bars, ± SD; n = 3, unpaired t test. ns, not significant. Scale bar, 100 μm.
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    MRTX1133 inhibits the growth of <t>PDAC</t> cells in “low”- but not “high”-confluent collagen cultures. A, PDAC cells (1 × 10 5 ) were grown in floating collagen gels (1.2 mg/mL) for 48 hours to generate “low”-confluent cultures. Depiction of “low”-confluent floating collagen cultures. B, PDAC cell lines (2138, 3213, 1245, <t>PANC1)</t> grown in “low”-confluent collagen cultures were treated with MRTX1133 (0.5 µmol/L) for 8 hours, and the effect on ERK1/2 phosphorylation was analyzed by Western blotting. Blots are representative of at least three biological replicates. C, PDAC cell lines grown in “low”-confluent collagen cultures were treated with DMSO or 0.5 µmol/L MRTX1133 for 72 hours. The cells were imaged at baseline and after 1, 2, and 3 days of treatment, and the relative growth was quantified. Error bars, ± SD; n = 3, unpaired t test. **, P < 0.01; ***, P < 0.001. Scale bar, 100 μm. D, PDAC cells (1 × 10 5 ) were grown in floating collagen gels (1.2 mg/mL) for 96 to 120 hours to generate “high-confluent” cultures. Depiction of “high-confluent” floating collagen cultures. E, PDAC cell lines grown in “high-confluent” collagen cultures were treated with MRTX1133 (0.5 µmol/L) for 8 hours, and the effect on ERK1/2 phosphorylation was analyzed by Western blotting. Blots are representative of at least three biological replicates. F, PDAC cell lines grown in “high-confluent” collagen cultures were treated with DMSO or 0.5 µmol/L MRTX1133 for 72 hours. The cells were imaged at baseline and after 1, 2, and 3 days of treatment, and the relative growth was quantified. Error bars, ± SD; n = 3, unpaired t test. ns, not significant. Scale bar, 100 μm.
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    MRTX1133 inhibits the growth of PDAC cells in “low”- but not “high”-confluent collagen cultures. A, PDAC cells (1 × 10 5 ) were grown in floating collagen gels (1.2 mg/mL) for 48 hours to generate “low”-confluent cultures. Depiction of “low”-confluent floating collagen cultures. B, PDAC cell lines (2138, 3213, 1245, PANC1) grown in “low”-confluent collagen cultures were treated with MRTX1133 (0.5 µmol/L) for 8 hours, and the effect on ERK1/2 phosphorylation was analyzed by Western blotting. Blots are representative of at least three biological replicates. C, PDAC cell lines grown in “low”-confluent collagen cultures were treated with DMSO or 0.5 µmol/L MRTX1133 for 72 hours. The cells were imaged at baseline and after 1, 2, and 3 days of treatment, and the relative growth was quantified. Error bars, ± SD; n = 3, unpaired t test. **, P < 0.01; ***, P < 0.001. Scale bar, 100 μm. D, PDAC cells (1 × 10 5 ) were grown in floating collagen gels (1.2 mg/mL) for 96 to 120 hours to generate “high-confluent” cultures. Depiction of “high-confluent” floating collagen cultures. E, PDAC cell lines grown in “high-confluent” collagen cultures were treated with MRTX1133 (0.5 µmol/L) for 8 hours, and the effect on ERK1/2 phosphorylation was analyzed by Western blotting. Blots are representative of at least three biological replicates. F, PDAC cell lines grown in “high-confluent” collagen cultures were treated with DMSO or 0.5 µmol/L MRTX1133 for 72 hours. The cells were imaged at baseline and after 1, 2, and 3 days of treatment, and the relative growth was quantified. Error bars, ± SD; n = 3, unpaired t test. ns, not significant. Scale bar, 100 μm.

    Journal: Cancer Research

    Article Title: Targeting BCL2 with Venetoclax Enhances the Efficacy of the KRAS G12D Inhibitor MRTX1133 in Pancreatic Cancer

    doi: 10.1158/0008-5472.CAN-23-3574

    Figure Lengend Snippet: MRTX1133 inhibits the growth of PDAC cells in “low”- but not “high”-confluent collagen cultures. A, PDAC cells (1 × 10 5 ) were grown in floating collagen gels (1.2 mg/mL) for 48 hours to generate “low”-confluent cultures. Depiction of “low”-confluent floating collagen cultures. B, PDAC cell lines (2138, 3213, 1245, PANC1) grown in “low”-confluent collagen cultures were treated with MRTX1133 (0.5 µmol/L) for 8 hours, and the effect on ERK1/2 phosphorylation was analyzed by Western blotting. Blots are representative of at least three biological replicates. C, PDAC cell lines grown in “low”-confluent collagen cultures were treated with DMSO or 0.5 µmol/L MRTX1133 for 72 hours. The cells were imaged at baseline and after 1, 2, and 3 days of treatment, and the relative growth was quantified. Error bars, ± SD; n = 3, unpaired t test. **, P < 0.01; ***, P < 0.001. Scale bar, 100 μm. D, PDAC cells (1 × 10 5 ) were grown in floating collagen gels (1.2 mg/mL) for 96 to 120 hours to generate “high-confluent” cultures. Depiction of “high-confluent” floating collagen cultures. E, PDAC cell lines grown in “high-confluent” collagen cultures were treated with MRTX1133 (0.5 µmol/L) for 8 hours, and the effect on ERK1/2 phosphorylation was analyzed by Western blotting. Blots are representative of at least three biological replicates. F, PDAC cell lines grown in “high-confluent” collagen cultures were treated with DMSO or 0.5 µmol/L MRTX1133 for 72 hours. The cells were imaged at baseline and after 1, 2, and 3 days of treatment, and the relative growth was quantified. Error bars, ± SD; n = 3, unpaired t test. ns, not significant. Scale bar, 100 μm.

    Article Snippet: The human PDAC cell line PANC1 was obtained from ATCC (CRL-1469).

    Techniques: Phospho-proteomics, Western Blot

    BCL2 inhibitor venetoclax enhances the efficacy of MRTX1133 in “high”-confluent collagen cultures. A, PDAC cells (2138, 3213, 1245, and PANC1) in “high”-confluent collagen cultures were treated with MRTX1133 (0.5 µmol/L) or the MEK1/2 inhibitor trametinib (0.1 µmol/L) for 8 hours. The effect on BIM and BCL2 was analyzed by Western blotting. Blots are representative of at least three biological replicates. B, PDAC cells in “high”-confluent collagen cultures were cotreated with venetoclax (2.5 µmol/L) and MRTX1133 (0.5 µmol/L) for 8 hours, and the effect on cell death (c-C3, cleaved-PARP) was analyzed. Blots are representative of at least three biological replicates. C, “High”-confluent collagen cultures of PDAC cells were cotreated with venetoclax (V; 2.5 µmol/L) and MRTX1133 (M; 0.5 µmol/L) for 48 hours, and the effect on cell growth was analyzed. Error bars, ± SD; n = 3 to 4. One-way ANOVA, followed by the Tukey multiple comparison test. D, PDAC cells were transfected with control siRNA or siRNA against BIM for 72 hours, plated in collagen, and treated with MRTX1133 (0.5 µmol/L) for 8 hours. The effect on BIM was analyzed using Western blotting. The transfected cells were also cotreated with venetoclax (2.5 µmol/L) and MRTX1133 (0.5 µmol/L) for 8 hours, and the effect on cell death (c-C3) was analyzed. Blots are representative of three biological replicates. E, “High”-confluent collagen cultures of PDAC cells were cotreated with venetoclax (2.5 µmol/L) and MRTX1133 (0.5 µmol/L) for 48 hours with or without the pan-caspase inhibitor zVAD-FMK (zVAD; 10 µmol/L), and the effect on cell growth was analyzed. Error bars, ± SD, n = 3. One-way ANOVA, followed by the Tukey multiple comparison test. **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

    Journal: Cancer Research

    Article Title: Targeting BCL2 with Venetoclax Enhances the Efficacy of the KRAS G12D Inhibitor MRTX1133 in Pancreatic Cancer

    doi: 10.1158/0008-5472.CAN-23-3574

    Figure Lengend Snippet: BCL2 inhibitor venetoclax enhances the efficacy of MRTX1133 in “high”-confluent collagen cultures. A, PDAC cells (2138, 3213, 1245, and PANC1) in “high”-confluent collagen cultures were treated with MRTX1133 (0.5 µmol/L) or the MEK1/2 inhibitor trametinib (0.1 µmol/L) for 8 hours. The effect on BIM and BCL2 was analyzed by Western blotting. Blots are representative of at least three biological replicates. B, PDAC cells in “high”-confluent collagen cultures were cotreated with venetoclax (2.5 µmol/L) and MRTX1133 (0.5 µmol/L) for 8 hours, and the effect on cell death (c-C3, cleaved-PARP) was analyzed. Blots are representative of at least three biological replicates. C, “High”-confluent collagen cultures of PDAC cells were cotreated with venetoclax (V; 2.5 µmol/L) and MRTX1133 (M; 0.5 µmol/L) for 48 hours, and the effect on cell growth was analyzed. Error bars, ± SD; n = 3 to 4. One-way ANOVA, followed by the Tukey multiple comparison test. D, PDAC cells were transfected with control siRNA or siRNA against BIM for 72 hours, plated in collagen, and treated with MRTX1133 (0.5 µmol/L) for 8 hours. The effect on BIM was analyzed using Western blotting. The transfected cells were also cotreated with venetoclax (2.5 µmol/L) and MRTX1133 (0.5 µmol/L) for 8 hours, and the effect on cell death (c-C3) was analyzed. Blots are representative of three biological replicates. E, “High”-confluent collagen cultures of PDAC cells were cotreated with venetoclax (2.5 µmol/L) and MRTX1133 (0.5 µmol/L) for 48 hours with or without the pan-caspase inhibitor zVAD-FMK (zVAD; 10 µmol/L), and the effect on cell growth was analyzed. Error bars, ± SD, n = 3. One-way ANOVA, followed by the Tukey multiple comparison test. **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

    Article Snippet: The human PDAC cell line PANC1 was obtained from ATCC (CRL-1469).

    Techniques: Western Blot, Comparison, Transfection, Control

    MRTX1133-resistant cells respond to the combination of MRTX1133 and venetoclax in collagen cultures. PDAC (2138, 3213, 1245, and PANC1) cells were treated over 6 to 8 weeks with increasing concentrations of MRTX1133 to 2 µmol/L or greater to generate PDAC-K cells. A, PDAC and PDAC-K cells growing on tissue culture plastic were treated with increasing concentrations of MRTX1133 for 8 hours, and ERK activation was evaluated by Western blotting. Blots are representative of three biological replicates. B, PDAC and PDAC-K cells grown in “low”-confluent collagen cultures were treated with DMSO or 2 µmol/L MRTX1133 for 72 hours. The cells were imaged at baseline and after 1, 2, and 3 days of treatment, the relative growth was quantified. Error bars, ± SD, n = 3. Unpaired t test. C, PDAC-K cells growing in “high”-confluent collagen cultures were treated with MRTX1133 (2 µmol/L), and the effect on pERK and BIM protein levels was analyzed by Western blotting. Blots are representative of three biological replicates. D, PDAC-K cells in “high”-confluent collagen cultures were treated with venetoclax (2.5 µmol/L) and MRTX1133 (2.0 µmol/L) for 8 hours, and the effect on cell death (c-C3 and cleaved-PARP) was analyzed. Blots are representative of at least three biological replicates. E, PDAC-K cells growing in “high”-confluent collagen cultures were cotreated with venetoclax (V; 2.5 µmol/L) and MRTX1133 (M; 2.0 µmol/L) for 48 hours, and the effect on cell growth was analyzed. Error bars, ± SD, n = 3. One-way ANOVA, followed by the Tukey multiple comparison test. *, P < 0.05; **, P < 0.01; ****, P < 0.0001.

    Journal: Cancer Research

    Article Title: Targeting BCL2 with Venetoclax Enhances the Efficacy of the KRAS G12D Inhibitor MRTX1133 in Pancreatic Cancer

    doi: 10.1158/0008-5472.CAN-23-3574

    Figure Lengend Snippet: MRTX1133-resistant cells respond to the combination of MRTX1133 and venetoclax in collagen cultures. PDAC (2138, 3213, 1245, and PANC1) cells were treated over 6 to 8 weeks with increasing concentrations of MRTX1133 to 2 µmol/L or greater to generate PDAC-K cells. A, PDAC and PDAC-K cells growing on tissue culture plastic were treated with increasing concentrations of MRTX1133 for 8 hours, and ERK activation was evaluated by Western blotting. Blots are representative of three biological replicates. B, PDAC and PDAC-K cells grown in “low”-confluent collagen cultures were treated with DMSO or 2 µmol/L MRTX1133 for 72 hours. The cells were imaged at baseline and after 1, 2, and 3 days of treatment, the relative growth was quantified. Error bars, ± SD, n = 3. Unpaired t test. C, PDAC-K cells growing in “high”-confluent collagen cultures were treated with MRTX1133 (2 µmol/L), and the effect on pERK and BIM protein levels was analyzed by Western blotting. Blots are representative of three biological replicates. D, PDAC-K cells in “high”-confluent collagen cultures were treated with venetoclax (2.5 µmol/L) and MRTX1133 (2.0 µmol/L) for 8 hours, and the effect on cell death (c-C3 and cleaved-PARP) was analyzed. Blots are representative of at least three biological replicates. E, PDAC-K cells growing in “high”-confluent collagen cultures were cotreated with venetoclax (V; 2.5 µmol/L) and MRTX1133 (M; 2.0 µmol/L) for 48 hours, and the effect on cell growth was analyzed. Error bars, ± SD, n = 3. One-way ANOVA, followed by the Tukey multiple comparison test. *, P < 0.05; **, P < 0.01; ****, P < 0.0001.

    Article Snippet: The human PDAC cell line PANC1 was obtained from ATCC (CRL-1469).

    Techniques: Activation Assay, Western Blot, Comparison