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human pdac cell lines  (ATCC)


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    Structured Review

    ATCC human pdac cell lines
    Glycolysis inhibitors diminish the virus sensitivity of glycolytic <t>PDAC</t> <t>cells</t> <t>MIA</t> PaCa-2 and PK-59 cells were treated with SCH772984 (SCH) (200 nM) or 2DG (2 mM), followed by infection with OBP-401 (100 MOI) or OBP-702 (10 MOI). (A) Lactate secretion by MIA PaCa-2 and PK-45H cells treated with SCH772984 or 2DG, presented as fold-increase compared with the control group, which was set as 1.0. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (B) Cell lysates of MIA PaCa-2 and PK-45H cells treated with SCH or 2DG for 48 h were subjected to western blot analysis for ERK1/2, GLUT1, and LDHA. (C) MIA PaCa-2 and PK-45H cells were treated with SCH or 2DG, followed by infection with OBP-401 (100 MOI) for 24 or 48 h. Upper panels show representative photographs of immunocytochemical staining for GFP in each group 48 h after infection. Scale bars, 500 μm. Lower graphs show the fluorescence intensity of GFP analyzed under fluorescence microscopy. Data are expressed as mean (SD) of independent experiment ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (D) MIA PaCa-2 and PK-45H cells were co-treated with OBP-702 and SCH772984 or 2DG at the indicated dose for 72 h. Cell viability was quantified using the XTT assay and calculated relative to the mock-infected group. Data are expressed as mean (SD) of independent experiment ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. (E) Cell lysates of MIA PaCa-2 and PK-45H cells co-treated with SCH or 2DG and OBP-702 (10 MOI) for 48 h were subjected to western blot analysis for E1A, p53, PARP, and cleaved C-PARP. β-actin was assayed as a loading control. The expression level of each protein was calculated relative to that of mock-treated cells, which was set at 1.0. N.S., not significant; ∗, p < 0.05.
    Human Pdac Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1281 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 97 stars, based on 1281 article reviews
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    Images

    1) Product Images from "Mitochondrial inhibition enhances the sensitivity of pancreatic ductal adenocarcinoma cells to oncolytic adenovirus"

    Article Title: Mitochondrial inhibition enhances the sensitivity of pancreatic ductal adenocarcinoma cells to oncolytic adenovirus

    Journal: Molecular Therapy Oncology

    doi: 10.1016/j.omton.2026.201180

    Glycolysis inhibitors diminish the virus sensitivity of glycolytic PDAC cells MIA PaCa-2 and PK-59 cells were treated with SCH772984 (SCH) (200 nM) or 2DG (2 mM), followed by infection with OBP-401 (100 MOI) or OBP-702 (10 MOI). (A) Lactate secretion by MIA PaCa-2 and PK-45H cells treated with SCH772984 or 2DG, presented as fold-increase compared with the control group, which was set as 1.0. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (B) Cell lysates of MIA PaCa-2 and PK-45H cells treated with SCH or 2DG for 48 h were subjected to western blot analysis for ERK1/2, GLUT1, and LDHA. (C) MIA PaCa-2 and PK-45H cells were treated with SCH or 2DG, followed by infection with OBP-401 (100 MOI) for 24 or 48 h. Upper panels show representative photographs of immunocytochemical staining for GFP in each group 48 h after infection. Scale bars, 500 μm. Lower graphs show the fluorescence intensity of GFP analyzed under fluorescence microscopy. Data are expressed as mean (SD) of independent experiment ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (D) MIA PaCa-2 and PK-45H cells were co-treated with OBP-702 and SCH772984 or 2DG at the indicated dose for 72 h. Cell viability was quantified using the XTT assay and calculated relative to the mock-infected group. Data are expressed as mean (SD) of independent experiment ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. (E) Cell lysates of MIA PaCa-2 and PK-45H cells co-treated with SCH or 2DG and OBP-702 (10 MOI) for 48 h were subjected to western blot analysis for E1A, p53, PARP, and cleaved C-PARP. β-actin was assayed as a loading control. The expression level of each protein was calculated relative to that of mock-treated cells, which was set at 1.0. N.S., not significant; ∗, p < 0.05.
    Figure Legend Snippet: Glycolysis inhibitors diminish the virus sensitivity of glycolytic PDAC cells MIA PaCa-2 and PK-59 cells were treated with SCH772984 (SCH) (200 nM) or 2DG (2 mM), followed by infection with OBP-401 (100 MOI) or OBP-702 (10 MOI). (A) Lactate secretion by MIA PaCa-2 and PK-45H cells treated with SCH772984 or 2DG, presented as fold-increase compared with the control group, which was set as 1.0. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (B) Cell lysates of MIA PaCa-2 and PK-45H cells treated with SCH or 2DG for 48 h were subjected to western blot analysis for ERK1/2, GLUT1, and LDHA. (C) MIA PaCa-2 and PK-45H cells were treated with SCH or 2DG, followed by infection with OBP-401 (100 MOI) for 24 or 48 h. Upper panels show representative photographs of immunocytochemical staining for GFP in each group 48 h after infection. Scale bars, 500 μm. Lower graphs show the fluorescence intensity of GFP analyzed under fluorescence microscopy. Data are expressed as mean (SD) of independent experiment ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (D) MIA PaCa-2 and PK-45H cells were co-treated with OBP-702 and SCH772984 or 2DG at the indicated dose for 72 h. Cell viability was quantified using the XTT assay and calculated relative to the mock-infected group. Data are expressed as mean (SD) of independent experiment ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. (E) Cell lysates of MIA PaCa-2 and PK-45H cells co-treated with SCH or 2DG and OBP-702 (10 MOI) for 48 h were subjected to western blot analysis for E1A, p53, PARP, and cleaved C-PARP. β-actin was assayed as a loading control. The expression level of each protein was calculated relative to that of mock-treated cells, which was set at 1.0. N.S., not significant; ∗, p < 0.05.

    Techniques Used: Virus, Infection, Control, Western Blot, Staining, Fluorescence, Microscopy, XTT Assay, Expressing

    p53 activation modulates glutamine metabolism in PDAC cells (A) Glutamine consumption in PDAC cells, presented as fold-increase compared with PBS, which was set as 1.0. (B) Outline of glutamine metabolism, shown from glutamine uptake to α-KG production. (C) Lysates of PDAC cells were subjected to western blot analysis for GDH1/2, OGDH, and IDH1. (D) PDAC cells were infected with OBP-301 or OBP-702 at an MOI of 100 for 48 h. The amount of intracellular α-KG in PDAC cells is shown as fold-increase compared with the mock-infected group, which was set as 1.0. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (E) PDAC cells were infected with OBP-301 or OBP-702 at the indicated MOIs for 72 h. Cell lysates were subjected to western blot analysis for GDH1/2, OGDH, and IDH1. (F) MIA PaCa-2 and PK-59 cells were infected with DL312 or Adp53 at the indicated MOIs for 24 h. The amount of intracellular αKG in PDAC cells is presented as fold-increase compared with mock-infected control groups. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences among four groups was determined using one-way ANOVA followed by Turkey’s multiple comparison procedure. (G) MIA PaCa-2 and PK-59 cells were infected with DL312 or Adp53 at the indicated MOIs for 48 h. Cell lysates were subjected to western blot analysis for p53, GDH1/2, OGDH, and IDH1. β-Actin was assayed as a loading control. The expression level of each protein was calculated relative to that of MIAPaCa-2 cells or mock-treated cells, which was set at 1.0. ∗, p < 0.05.
    Figure Legend Snippet: p53 activation modulates glutamine metabolism in PDAC cells (A) Glutamine consumption in PDAC cells, presented as fold-increase compared with PBS, which was set as 1.0. (B) Outline of glutamine metabolism, shown from glutamine uptake to α-KG production. (C) Lysates of PDAC cells were subjected to western blot analysis for GDH1/2, OGDH, and IDH1. (D) PDAC cells were infected with OBP-301 or OBP-702 at an MOI of 100 for 48 h. The amount of intracellular α-KG in PDAC cells is shown as fold-increase compared with the mock-infected group, which was set as 1.0. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (E) PDAC cells were infected with OBP-301 or OBP-702 at the indicated MOIs for 72 h. Cell lysates were subjected to western blot analysis for GDH1/2, OGDH, and IDH1. (F) MIA PaCa-2 and PK-59 cells were infected with DL312 or Adp53 at the indicated MOIs for 24 h. The amount of intracellular αKG in PDAC cells is presented as fold-increase compared with mock-infected control groups. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences among four groups was determined using one-way ANOVA followed by Turkey’s multiple comparison procedure. (G) MIA PaCa-2 and PK-59 cells were infected with DL312 or Adp53 at the indicated MOIs for 48 h. Cell lysates were subjected to western blot analysis for p53, GDH1/2, OGDH, and IDH1. β-Actin was assayed as a loading control. The expression level of each protein was calculated relative to that of MIAPaCa-2 cells or mock-treated cells, which was set at 1.0. ∗, p < 0.05.

    Techniques Used: Activation Assay, Western Blot, Infection, Control, Comparison, Expressing

    Comparison of metabolic phenotypes and virus sensitivity in subcutaneous tumor models with glycolytic and non-glycolytic PDAC cells (A) Representative photographs of immunohistochemical staining for LDHA, GLUT1, and IDH1 in each group. Scale bars, 100 μm. (B) Expression levels of LDHA, GLUT1, and IDH1, calculated by dividing the DAB intensity by the number of cells in randomly selected fields. Data are expressed as mean (SD) of independent experiments ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. (C) MIA PaCa-2 tumor-bearing mice received intratumoral injections of PBS (black arrows) or OBP-702 (green arrows) every other day for 3 cycles. Data are expressed as mean (SD) of independent experiments ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. (D) PK-59 tumor-bearing mice received intratumoral injections of PBS (black arrows) or OBP-702 (orange arrows). The upper right photographs show tumor-bearing mice in the control and OBP-702-treated groups. The lower right photographs show tumors in the mock and OBP-702 groups. Data are expressed as mean (SD) of independent experiments ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. ∗, p < 0.05.
    Figure Legend Snippet: Comparison of metabolic phenotypes and virus sensitivity in subcutaneous tumor models with glycolytic and non-glycolytic PDAC cells (A) Representative photographs of immunohistochemical staining for LDHA, GLUT1, and IDH1 in each group. Scale bars, 100 μm. (B) Expression levels of LDHA, GLUT1, and IDH1, calculated by dividing the DAB intensity by the number of cells in randomly selected fields. Data are expressed as mean (SD) of independent experiments ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. (C) MIA PaCa-2 tumor-bearing mice received intratumoral injections of PBS (black arrows) or OBP-702 (green arrows) every other day for 3 cycles. Data are expressed as mean (SD) of independent experiments ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. (D) PK-59 tumor-bearing mice received intratumoral injections of PBS (black arrows) or OBP-702 (orange arrows). The upper right photographs show tumor-bearing mice in the control and OBP-702-treated groups. The lower right photographs show tumors in the mock and OBP-702 groups. Data are expressed as mean (SD) of independent experiments ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. ∗, p < 0.05.

    Techniques Used: Comparison, Virus, Immunohistochemical staining, Staining, Expressing, Control

    Investigation of the relationship between PET/CT metabolic parameters and glycolytic activity of PDAC tumors (A and B) PET/CT images of MIA PaCa-2 tumor (A) and PK-59 tumor (B). The upper left (a) shows the horizontal section, whereas the lower left (b) shows the sagittal section, and the right (c) shows the coronal section. Dotted circles indicate the tumor area. (C) Comparison of SUVmax values for MIA PaCa-2 and PK-59 tumors. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (D and E) Comparison of MTV (D) and TLG (E) values for MIA PaCa-2 and PK-59 tumors at the indicated thresholds. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (F and G) Scatter diagrams demonstrating correlations between expression of LDHA (F) or GLUT1 (G) and preoperative SUVmax (left), MTV (40%) (center), and TLG (40%) (right) values in patients with PDAC ( n = 30). The statistical significance of the correlations in the scatterplots was determined using Pearson’s correlation analysis. N.S., not significant; ∗, p < 0.05.
    Figure Legend Snippet: Investigation of the relationship between PET/CT metabolic parameters and glycolytic activity of PDAC tumors (A and B) PET/CT images of MIA PaCa-2 tumor (A) and PK-59 tumor (B). The upper left (a) shows the horizontal section, whereas the lower left (b) shows the sagittal section, and the right (c) shows the coronal section. Dotted circles indicate the tumor area. (C) Comparison of SUVmax values for MIA PaCa-2 and PK-59 tumors. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (D and E) Comparison of MTV (D) and TLG (E) values for MIA PaCa-2 and PK-59 tumors at the indicated thresholds. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (F and G) Scatter diagrams demonstrating correlations between expression of LDHA (F) or GLUT1 (G) and preoperative SUVmax (left), MTV (40%) (center), and TLG (40%) (right) values in patients with PDAC ( n = 30). The statistical significance of the correlations in the scatterplots was determined using Pearson’s correlation analysis. N.S., not significant; ∗, p < 0.05.

    Techniques Used: Positron Emission Tomography-Computed Tomography, Activity Assay, Comparison, Expressing

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    Article Snippet: Tetraspanin 7 (TSPAN7) plays a crucial role in cancer progression; however, its correlation with pancreatic ductal adenocarcinoma (PDAC) remains unclear.. This study aimed to analyse TSPAN7 expression and prognostic value in PDAC by integrating data from public databases and our PDAC cohort.. We evaluated the effect of TSPAN7 on PDAC cell proliferation and apoptosis using cell-based assays and mouse xenograft models.

    Article Title: ALDH1A3 promotes the lung metastatic organotropism of pancreatic ductal adenocarcinoma through semaphorin signaling.
    Article Snippet: All PDAC cells were cultured in DMEM (319-005- CL, Wisent) supplemented with 10% fetal bovine serum (FBS, 04-001-1A, Biological Industries) at 37◦C with 5% CO2. .. The PDAC cell lines (HPAC and Aspc-1) and murine lung epithelial cell line MLE-12 were purchased from ATCC (Beijing, China) and cultured in DMEM supplemented with 5% FBS. ..



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    Procell Inc human pdac cell lines capan 1
    Glycolysis inhibitors diminish the virus sensitivity of glycolytic <t>PDAC</t> <t>cells</t> <t>MIA</t> PaCa-2 and PK-59 cells were treated with SCH772984 (SCH) (200 nM) or 2DG (2 mM), followed by infection with OBP-401 (100 MOI) or OBP-702 (10 MOI). (A) Lactate secretion by MIA PaCa-2 and PK-45H cells treated with SCH772984 or 2DG, presented as fold-increase compared with the control group, which was set as 1.0. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (B) Cell lysates of MIA PaCa-2 and PK-45H cells treated with SCH or 2DG for 48 h were subjected to western blot analysis for ERK1/2, GLUT1, and LDHA. (C) MIA PaCa-2 and PK-45H cells were treated with SCH or 2DG, followed by infection with OBP-401 (100 MOI) for 24 or 48 h. Upper panels show representative photographs of immunocytochemical staining for GFP in each group 48 h after infection. Scale bars, 500 μm. Lower graphs show the fluorescence intensity of GFP analyzed under fluorescence microscopy. Data are expressed as mean (SD) of independent experiment ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (D) MIA PaCa-2 and PK-45H cells were co-treated with OBP-702 and SCH772984 or 2DG at the indicated dose for 72 h. Cell viability was quantified using the XTT assay and calculated relative to the mock-infected group. Data are expressed as mean (SD) of independent experiment ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. (E) Cell lysates of MIA PaCa-2 and PK-45H cells co-treated with SCH or 2DG and OBP-702 (10 MOI) for 48 h were subjected to western blot analysis for E1A, p53, PARP, and cleaved C-PARP. β-actin was assayed as a loading control. The expression level of each protein was calculated relative to that of mock-treated cells, which was set at 1.0. N.S., not significant; ∗, p < 0.05.
    Human Pdac Cell Lines Capan 1, supplied by Procell Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC pancreatic adenocarcinoma pdac cell line panc 1
    Glycolysis inhibitors diminish the virus sensitivity of glycolytic <t>PDAC</t> <t>cells</t> <t>MIA</t> PaCa-2 and PK-59 cells were treated with SCH772984 (SCH) (200 nM) or 2DG (2 mM), followed by infection with OBP-401 (100 MOI) or OBP-702 (10 MOI). (A) Lactate secretion by MIA PaCa-2 and PK-45H cells treated with SCH772984 or 2DG, presented as fold-increase compared with the control group, which was set as 1.0. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (B) Cell lysates of MIA PaCa-2 and PK-45H cells treated with SCH or 2DG for 48 h were subjected to western blot analysis for ERK1/2, GLUT1, and LDHA. (C) MIA PaCa-2 and PK-45H cells were treated with SCH or 2DG, followed by infection with OBP-401 (100 MOI) for 24 or 48 h. Upper panels show representative photographs of immunocytochemical staining for GFP in each group 48 h after infection. Scale bars, 500 μm. Lower graphs show the fluorescence intensity of GFP analyzed under fluorescence microscopy. Data are expressed as mean (SD) of independent experiment ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (D) MIA PaCa-2 and PK-45H cells were co-treated with OBP-702 and SCH772984 or 2DG at the indicated dose for 72 h. Cell viability was quantified using the XTT assay and calculated relative to the mock-infected group. Data are expressed as mean (SD) of independent experiment ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. (E) Cell lysates of MIA PaCa-2 and PK-45H cells co-treated with SCH or 2DG and OBP-702 (10 MOI) for 48 h were subjected to western blot analysis for E1A, p53, PARP, and cleaved C-PARP. β-actin was assayed as a loading control. The expression level of each protein was calculated relative to that of mock-treated cells, which was set at 1.0. N.S., not significant; ∗, p < 0.05.
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    ATCC pdac cell lines
    Glycolysis inhibitors diminish the virus sensitivity of glycolytic <t>PDAC</t> <t>cells</t> <t>MIA</t> PaCa-2 and PK-59 cells were treated with SCH772984 (SCH) (200 nM) or 2DG (2 mM), followed by infection with OBP-401 (100 MOI) or OBP-702 (10 MOI). (A) Lactate secretion by MIA PaCa-2 and PK-45H cells treated with SCH772984 or 2DG, presented as fold-increase compared with the control group, which was set as 1.0. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (B) Cell lysates of MIA PaCa-2 and PK-45H cells treated with SCH or 2DG for 48 h were subjected to western blot analysis for ERK1/2, GLUT1, and LDHA. (C) MIA PaCa-2 and PK-45H cells were treated with SCH or 2DG, followed by infection with OBP-401 (100 MOI) for 24 or 48 h. Upper panels show representative photographs of immunocytochemical staining for GFP in each group 48 h after infection. Scale bars, 500 μm. Lower graphs show the fluorescence intensity of GFP analyzed under fluorescence microscopy. Data are expressed as mean (SD) of independent experiment ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (D) MIA PaCa-2 and PK-45H cells were co-treated with OBP-702 and SCH772984 or 2DG at the indicated dose for 72 h. Cell viability was quantified using the XTT assay and calculated relative to the mock-infected group. Data are expressed as mean (SD) of independent experiment ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. (E) Cell lysates of MIA PaCa-2 and PK-45H cells co-treated with SCH or 2DG and OBP-702 (10 MOI) for 48 h were subjected to western blot analysis for E1A, p53, PARP, and cleaved C-PARP. β-actin was assayed as a loading control. The expression level of each protein was calculated relative to that of mock-treated cells, which was set at 1.0. N.S., not significant; ∗, p < 0.05.
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    ATCC pdac cell lines panc 1
    Glycolysis inhibitors diminish the virus sensitivity of glycolytic <t>PDAC</t> <t>cells</t> <t>MIA</t> PaCa-2 and PK-59 cells were treated with SCH772984 (SCH) (200 nM) or 2DG (2 mM), followed by infection with OBP-401 (100 MOI) or OBP-702 (10 MOI). (A) Lactate secretion by MIA PaCa-2 and PK-45H cells treated with SCH772984 or 2DG, presented as fold-increase compared with the control group, which was set as 1.0. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (B) Cell lysates of MIA PaCa-2 and PK-45H cells treated with SCH or 2DG for 48 h were subjected to western blot analysis for ERK1/2, GLUT1, and LDHA. (C) MIA PaCa-2 and PK-45H cells were treated with SCH or 2DG, followed by infection with OBP-401 (100 MOI) for 24 or 48 h. Upper panels show representative photographs of immunocytochemical staining for GFP in each group 48 h after infection. Scale bars, 500 μm. Lower graphs show the fluorescence intensity of GFP analyzed under fluorescence microscopy. Data are expressed as mean (SD) of independent experiment ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (D) MIA PaCa-2 and PK-45H cells were co-treated with OBP-702 and SCH772984 or 2DG at the indicated dose for 72 h. Cell viability was quantified using the XTT assay and calculated relative to the mock-infected group. Data are expressed as mean (SD) of independent experiment ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. (E) Cell lysates of MIA PaCa-2 and PK-45H cells co-treated with SCH or 2DG and OBP-702 (10 MOI) for 48 h were subjected to western blot analysis for E1A, p53, PARP, and cleaved C-PARP. β-actin was assayed as a loading control. The expression level of each protein was calculated relative to that of mock-treated cells, which was set at 1.0. N.S., not significant; ∗, p < 0.05.
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    ATCC pdac cell lines aspc 1
    Glycolysis inhibitors diminish the virus sensitivity of glycolytic <t>PDAC</t> <t>cells</t> <t>MIA</t> PaCa-2 and PK-59 cells were treated with SCH772984 (SCH) (200 nM) or 2DG (2 mM), followed by infection with OBP-401 (100 MOI) or OBP-702 (10 MOI). (A) Lactate secretion by MIA PaCa-2 and PK-45H cells treated with SCH772984 or 2DG, presented as fold-increase compared with the control group, which was set as 1.0. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (B) Cell lysates of MIA PaCa-2 and PK-45H cells treated with SCH or 2DG for 48 h were subjected to western blot analysis for ERK1/2, GLUT1, and LDHA. (C) MIA PaCa-2 and PK-45H cells were treated with SCH or 2DG, followed by infection with OBP-401 (100 MOI) for 24 or 48 h. Upper panels show representative photographs of immunocytochemical staining for GFP in each group 48 h after infection. Scale bars, 500 μm. Lower graphs show the fluorescence intensity of GFP analyzed under fluorescence microscopy. Data are expressed as mean (SD) of independent experiment ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (D) MIA PaCa-2 and PK-45H cells were co-treated with OBP-702 and SCH772984 or 2DG at the indicated dose for 72 h. Cell viability was quantified using the XTT assay and calculated relative to the mock-infected group. Data are expressed as mean (SD) of independent experiment ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. (E) Cell lysates of MIA PaCa-2 and PK-45H cells co-treated with SCH or 2DG and OBP-702 (10 MOI) for 48 h were subjected to western blot analysis for E1A, p53, PARP, and cleaved C-PARP. β-actin was assayed as a loading control. The expression level of each protein was calculated relative to that of mock-treated cells, which was set at 1.0. N.S., not significant; ∗, p < 0.05.
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    Glycolysis inhibitors diminish the virus sensitivity of glycolytic PDAC cells MIA PaCa-2 and PK-59 cells were treated with SCH772984 (SCH) (200 nM) or 2DG (2 mM), followed by infection with OBP-401 (100 MOI) or OBP-702 (10 MOI). (A) Lactate secretion by MIA PaCa-2 and PK-45H cells treated with SCH772984 or 2DG, presented as fold-increase compared with the control group, which was set as 1.0. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (B) Cell lysates of MIA PaCa-2 and PK-45H cells treated with SCH or 2DG for 48 h were subjected to western blot analysis for ERK1/2, GLUT1, and LDHA. (C) MIA PaCa-2 and PK-45H cells were treated with SCH or 2DG, followed by infection with OBP-401 (100 MOI) for 24 or 48 h. Upper panels show representative photographs of immunocytochemical staining for GFP in each group 48 h after infection. Scale bars, 500 μm. Lower graphs show the fluorescence intensity of GFP analyzed under fluorescence microscopy. Data are expressed as mean (SD) of independent experiment ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (D) MIA PaCa-2 and PK-45H cells were co-treated with OBP-702 and SCH772984 or 2DG at the indicated dose for 72 h. Cell viability was quantified using the XTT assay and calculated relative to the mock-infected group. Data are expressed as mean (SD) of independent experiment ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. (E) Cell lysates of MIA PaCa-2 and PK-45H cells co-treated with SCH or 2DG and OBP-702 (10 MOI) for 48 h were subjected to western blot analysis for E1A, p53, PARP, and cleaved C-PARP. β-actin was assayed as a loading control. The expression level of each protein was calculated relative to that of mock-treated cells, which was set at 1.0. N.S., not significant; ∗, p < 0.05.

    Journal: Molecular Therapy Oncology

    Article Title: Mitochondrial inhibition enhances the sensitivity of pancreatic ductal adenocarcinoma cells to oncolytic adenovirus

    doi: 10.1016/j.omton.2026.201180

    Figure Lengend Snippet: Glycolysis inhibitors diminish the virus sensitivity of glycolytic PDAC cells MIA PaCa-2 and PK-59 cells were treated with SCH772984 (SCH) (200 nM) or 2DG (2 mM), followed by infection with OBP-401 (100 MOI) or OBP-702 (10 MOI). (A) Lactate secretion by MIA PaCa-2 and PK-45H cells treated with SCH772984 or 2DG, presented as fold-increase compared with the control group, which was set as 1.0. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (B) Cell lysates of MIA PaCa-2 and PK-45H cells treated with SCH or 2DG for 48 h were subjected to western blot analysis for ERK1/2, GLUT1, and LDHA. (C) MIA PaCa-2 and PK-45H cells were treated with SCH or 2DG, followed by infection with OBP-401 (100 MOI) for 24 or 48 h. Upper panels show representative photographs of immunocytochemical staining for GFP in each group 48 h after infection. Scale bars, 500 μm. Lower graphs show the fluorescence intensity of GFP analyzed under fluorescence microscopy. Data are expressed as mean (SD) of independent experiment ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (D) MIA PaCa-2 and PK-45H cells were co-treated with OBP-702 and SCH772984 or 2DG at the indicated dose for 72 h. Cell viability was quantified using the XTT assay and calculated relative to the mock-infected group. Data are expressed as mean (SD) of independent experiment ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. (E) Cell lysates of MIA PaCa-2 and PK-45H cells co-treated with SCH or 2DG and OBP-702 (10 MOI) for 48 h were subjected to western blot analysis for E1A, p53, PARP, and cleaved C-PARP. β-actin was assayed as a loading control. The expression level of each protein was calculated relative to that of mock-treated cells, which was set at 1.0. N.S., not significant; ∗, p < 0.05.

    Article Snippet: Two human PDAC cell lines (MIA PaCa-2 and Capan-2) were obtained from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: Virus, Infection, Control, Western Blot, Staining, Fluorescence, Microscopy, XTT Assay, Expressing

    p53 activation modulates glutamine metabolism in PDAC cells (A) Glutamine consumption in PDAC cells, presented as fold-increase compared with PBS, which was set as 1.0. (B) Outline of glutamine metabolism, shown from glutamine uptake to α-KG production. (C) Lysates of PDAC cells were subjected to western blot analysis for GDH1/2, OGDH, and IDH1. (D) PDAC cells were infected with OBP-301 or OBP-702 at an MOI of 100 for 48 h. The amount of intracellular α-KG in PDAC cells is shown as fold-increase compared with the mock-infected group, which was set as 1.0. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (E) PDAC cells were infected with OBP-301 or OBP-702 at the indicated MOIs for 72 h. Cell lysates were subjected to western blot analysis for GDH1/2, OGDH, and IDH1. (F) MIA PaCa-2 and PK-59 cells were infected with DL312 or Adp53 at the indicated MOIs for 24 h. The amount of intracellular αKG in PDAC cells is presented as fold-increase compared with mock-infected control groups. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences among four groups was determined using one-way ANOVA followed by Turkey’s multiple comparison procedure. (G) MIA PaCa-2 and PK-59 cells were infected with DL312 or Adp53 at the indicated MOIs for 48 h. Cell lysates were subjected to western blot analysis for p53, GDH1/2, OGDH, and IDH1. β-Actin was assayed as a loading control. The expression level of each protein was calculated relative to that of MIAPaCa-2 cells or mock-treated cells, which was set at 1.0. ∗, p < 0.05.

    Journal: Molecular Therapy Oncology

    Article Title: Mitochondrial inhibition enhances the sensitivity of pancreatic ductal adenocarcinoma cells to oncolytic adenovirus

    doi: 10.1016/j.omton.2026.201180

    Figure Lengend Snippet: p53 activation modulates glutamine metabolism in PDAC cells (A) Glutamine consumption in PDAC cells, presented as fold-increase compared with PBS, which was set as 1.0. (B) Outline of glutamine metabolism, shown from glutamine uptake to α-KG production. (C) Lysates of PDAC cells were subjected to western blot analysis for GDH1/2, OGDH, and IDH1. (D) PDAC cells were infected with OBP-301 or OBP-702 at an MOI of 100 for 48 h. The amount of intracellular α-KG in PDAC cells is shown as fold-increase compared with the mock-infected group, which was set as 1.0. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (E) PDAC cells were infected with OBP-301 or OBP-702 at the indicated MOIs for 72 h. Cell lysates were subjected to western blot analysis for GDH1/2, OGDH, and IDH1. (F) MIA PaCa-2 and PK-59 cells were infected with DL312 or Adp53 at the indicated MOIs for 24 h. The amount of intracellular αKG in PDAC cells is presented as fold-increase compared with mock-infected control groups. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences among four groups was determined using one-way ANOVA followed by Turkey’s multiple comparison procedure. (G) MIA PaCa-2 and PK-59 cells were infected with DL312 or Adp53 at the indicated MOIs for 48 h. Cell lysates were subjected to western blot analysis for p53, GDH1/2, OGDH, and IDH1. β-Actin was assayed as a loading control. The expression level of each protein was calculated relative to that of MIAPaCa-2 cells or mock-treated cells, which was set at 1.0. ∗, p < 0.05.

    Article Snippet: Two human PDAC cell lines (MIA PaCa-2 and Capan-2) were obtained from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: Activation Assay, Western Blot, Infection, Control, Comparison, Expressing

    Comparison of metabolic phenotypes and virus sensitivity in subcutaneous tumor models with glycolytic and non-glycolytic PDAC cells (A) Representative photographs of immunohistochemical staining for LDHA, GLUT1, and IDH1 in each group. Scale bars, 100 μm. (B) Expression levels of LDHA, GLUT1, and IDH1, calculated by dividing the DAB intensity by the number of cells in randomly selected fields. Data are expressed as mean (SD) of independent experiments ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. (C) MIA PaCa-2 tumor-bearing mice received intratumoral injections of PBS (black arrows) or OBP-702 (green arrows) every other day for 3 cycles. Data are expressed as mean (SD) of independent experiments ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. (D) PK-59 tumor-bearing mice received intratumoral injections of PBS (black arrows) or OBP-702 (orange arrows). The upper right photographs show tumor-bearing mice in the control and OBP-702-treated groups. The lower right photographs show tumors in the mock and OBP-702 groups. Data are expressed as mean (SD) of independent experiments ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. ∗, p < 0.05.

    Journal: Molecular Therapy Oncology

    Article Title: Mitochondrial inhibition enhances the sensitivity of pancreatic ductal adenocarcinoma cells to oncolytic adenovirus

    doi: 10.1016/j.omton.2026.201180

    Figure Lengend Snippet: Comparison of metabolic phenotypes and virus sensitivity in subcutaneous tumor models with glycolytic and non-glycolytic PDAC cells (A) Representative photographs of immunohistochemical staining for LDHA, GLUT1, and IDH1 in each group. Scale bars, 100 μm. (B) Expression levels of LDHA, GLUT1, and IDH1, calculated by dividing the DAB intensity by the number of cells in randomly selected fields. Data are expressed as mean (SD) of independent experiments ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. (C) MIA PaCa-2 tumor-bearing mice received intratumoral injections of PBS (black arrows) or OBP-702 (green arrows) every other day for 3 cycles. Data are expressed as mean (SD) of independent experiments ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. (D) PK-59 tumor-bearing mice received intratumoral injections of PBS (black arrows) or OBP-702 (orange arrows). The upper right photographs show tumor-bearing mice in the control and OBP-702-treated groups. The lower right photographs show tumors in the mock and OBP-702 groups. Data are expressed as mean (SD) of independent experiments ( n = 5). The statistical significance of differences between two groups was determined using the Student’s t test. ∗, p < 0.05.

    Article Snippet: Two human PDAC cell lines (MIA PaCa-2 and Capan-2) were obtained from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: Comparison, Virus, Immunohistochemical staining, Staining, Expressing, Control

    Investigation of the relationship between PET/CT metabolic parameters and glycolytic activity of PDAC tumors (A and B) PET/CT images of MIA PaCa-2 tumor (A) and PK-59 tumor (B). The upper left (a) shows the horizontal section, whereas the lower left (b) shows the sagittal section, and the right (c) shows the coronal section. Dotted circles indicate the tumor area. (C) Comparison of SUVmax values for MIA PaCa-2 and PK-59 tumors. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (D and E) Comparison of MTV (D) and TLG (E) values for MIA PaCa-2 and PK-59 tumors at the indicated thresholds. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (F and G) Scatter diagrams demonstrating correlations between expression of LDHA (F) or GLUT1 (G) and preoperative SUVmax (left), MTV (40%) (center), and TLG (40%) (right) values in patients with PDAC ( n = 30). The statistical significance of the correlations in the scatterplots was determined using Pearson’s correlation analysis. N.S., not significant; ∗, p < 0.05.

    Journal: Molecular Therapy Oncology

    Article Title: Mitochondrial inhibition enhances the sensitivity of pancreatic ductal adenocarcinoma cells to oncolytic adenovirus

    doi: 10.1016/j.omton.2026.201180

    Figure Lengend Snippet: Investigation of the relationship between PET/CT metabolic parameters and glycolytic activity of PDAC tumors (A and B) PET/CT images of MIA PaCa-2 tumor (A) and PK-59 tumor (B). The upper left (a) shows the horizontal section, whereas the lower left (b) shows the sagittal section, and the right (c) shows the coronal section. Dotted circles indicate the tumor area. (C) Comparison of SUVmax values for MIA PaCa-2 and PK-59 tumors. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (D and E) Comparison of MTV (D) and TLG (E) values for MIA PaCa-2 and PK-59 tumors at the indicated thresholds. Data are expressed as mean (SD) of independent experiments ( n = 3). The statistical significance of differences between two groups was determined using the Student’s t test. (F and G) Scatter diagrams demonstrating correlations between expression of LDHA (F) or GLUT1 (G) and preoperative SUVmax (left), MTV (40%) (center), and TLG (40%) (right) values in patients with PDAC ( n = 30). The statistical significance of the correlations in the scatterplots was determined using Pearson’s correlation analysis. N.S., not significant; ∗, p < 0.05.

    Article Snippet: Two human PDAC cell lines (MIA PaCa-2 and Capan-2) were obtained from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: Positron Emission Tomography-Computed Tomography, Activity Assay, Comparison, Expressing