miapaca 2 cells  (ATCC)

Journal: Materials Today Bio

Article Title: Escape from cell uptake: Drug-Free cancer therapeutics regulated by hydrophobicity and negative charge

doi: 10.1016/j.mtbio.2025.102752

Figure Lengend Snippet: Cytotoxicity and Cell adsorption property of PVA-U varying G.D. (a) IC 50 values of MIAPaCa-2 cells treated with UDCA, PVA-U3, PVA-U15, and PVA-U25 for 24 h incubation at pH 7.4 and pH 6.5 (n = 3). (b) Cell viability of MIAPaCa-2 cells treated with 10 μg mL −1 PVA-U15 at pH 7.4 and pH 6.5 for 0, 4, 12, and 24 h incubation (n = 3). (c) Confocal images of MIAPaCa-2 cells treated with Cell tracker deep red and 10 μg mL −1 PVA-U0-R, PVA-U3-R, PVA-U15-R, and PVA-U25-R at pH 7.4 and pH 6.5 for 12 h incubation. Cell tracker deep red and PVA-Us were shown in green and red color, respectively. Scale bars of images and enlarge images are 100 μm and 50 μm, respectively. Quantification of intracellular fluorescence intensity of MIAPaCa-2 cells treated with PVA-U0 (black), PVA-U3 (light blue), PVA-U15 (blue), and PVA-U25 (dark blue) incubated for 24 h at pH 7.4 (d) and pH 6.5 (e) (n = 11). Quantification of pericellular fluorescence intensity of MIAPaCa-2 cells treated with PVA-U0 (black), PVA-U3 (light blue), PVA-U15 (blue), and PVA-U25 (dark blue) incubated for 4 h at pH 7.4 (f) and pH 6.5 (g) (n = 11). (h) Confocal images of MIAPaCa-2 cells treated with lysotracker and 10 μg mL −1 PVA-U0-R, PVA-U3-R, PVA-U15-R, and PVA-U25-R at pH 6.5 for 4 h incubation. Lysotracker deep red and PVA-Us were shown in green and red color, respectively. Scale bars of images and enlarge images are 50 μm and 10 μm, respectively. Statistical analysis was performed using unpaired two-tailed Student's t -test. Data are presented as mean ± S.D. ( N.S. : no significant difference, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001).

Article Snippet: MIAPaCa-2 cells, HT-29 cells, and A549 cells were purchased from the American Type Culture Collection (Manassas, VA, USA).

Techniques: Adsorption, Incubation, Fluorescence, Two Tailed Test

Journal: Materials Today Bio

Article Title: Escape from cell uptake: Drug-Free cancer therapeutics regulated by hydrophobicity and negative charge

doi: 10.1016/j.mtbio.2025.102752

Figure Lengend Snippet: Antitumor efficacy of PVA-U15. (a) Treatment schedule for MIAPaCa-2 tumors. BALB/c nude mice were inoculated with MIAPaCa-2 cells on day 0. The tumor-bearing mice were randomized and treated with UDCA (144 μM), PVA (10 μg mL −1 ) or PVA-U15 (10 μg mL −1 ). 100 μL of each solution was intratumorally injected 5 days per week from day 9 to day 21. (b) Tumor growth in mice treated with PVA (black), UDCA (blue), and PVA-U15 (red). (c) Body weight of mice treated with PVA (black), UDCA (blue), and PVA-U15 (red). Statistical analysis was performed using Tukey test. Data are presented as mean ± S.D. (∗ p < 0.05).

Article Snippet: MIAPaCa-2 cells, HT-29 cells, and A549 cells were purchased from the American Type Culture Collection (Manassas, VA, USA).

Techniques: Injection

Journal: bioRxiv

Article Title: DHHC7 palmitoylates KRAS4A and promotes mutant KRAS-driven pancreatic cancers

doi: 10.64898/2026.03.31.715686

Figure Lengend Snippet: ( a, b ) DHHC7 promotes pERK and 2-D cell growth of pancreatic cancer cells. ZDHHC7 was knockdown using siRNA in four mutant KRAS-driven pancreatic cancer cell lines (AsPC1, MiaPaca-2, PANC0327 and Tu8988s) ( a ) and one non-KRAS driven pancreatic cancer cell line (BxPC3) ( b ). pERK was measured using western blot and 2-D cell growth was measured using Cell Titer Glow after 48-72 hrs. ( c-d ) ZDHHC7 knockout affects pERK, 2-D cell growth, KRAS4A S-palmitoylation in MiaPaca-2 cell line. ZDHHC7 was CRISPR knockout and pERK levels ( c ) were detected using western blot and 2D cell growth was measured after 72 hrs. The endogenous S-acylation level of KRAS4A was detected using ABE ( d ). ( e ) ZDHHC7 was CRISPR knockout in AsPC1 cell line and pERK levels were detected using western blot. ( f-h ) ZDHHC7 knockout suppresses MiaPaca-2 xenograft tumor growth. Pancreatic cancer xerograph was performed using MiaPaca-2 cells with control or ZDHHC7 CRISPR knockout. The tumor volume was measured and quantified (f). The mice were dissected, and the final tumors were shown ( g ) and the tumor weights were quantified ( h ). ( i-k ) ZDHHC7 knockout suppresses AsPC1 xenograft tumor growth. ZDHHC7 CRISPR knockout was performed in AsPC1 cell line and similar xenograft experiment was performed. Tumor volume (i), tumors (j), tumor weight (k) are shown. Quantification data are shown as mean ± SD. ns, not significant. * P < 0.05; ** P < 0.01; *** P < 0.001.

Article Snippet: Tumors were established by subcutaneously injecting MiaPaca-2 cells (3 × 10^6 cells per animal), PANC 0327 cells (1 x 10^6 cells per animal), AsPC1 cells (1 x 10^6 cells per animal) and BxPC3 cells (1 x 10^6 cells per animal) into 4- to 6-week-old male NSG mice (Jackson Laboratory, Bar Harbor, US).

Techniques: Knockdown, Mutagenesis, Western Blot, Knock-Out, CRISPR, Control

Journal: Advanced Science

Article Title: An Insulin‐Exosome‐TNFAIP8 Axis Drives Stromal Fibrosis and Therapeutic Resistance in Pancreatic Cancer

doi: 10.1002/advs.202515606

Figure Lengend Snippet: TNFAIP8 is enriched in insulin‐stimulated PDAC exosomes and promotes CAF activation. (A) Heatmap of differentially expressed proteins in exosomes from insulin‐treated versus control MIA PaCa‐2 cells. (B) KEGG pathway enrichment analysis of upregulated exosomal proteins. (C) Expression of TNFAIP8 based on normalized TCGA‐PAAD data. (D) Forest plot summarizing Cox regression analyses linking TNFAIP8 expression to survival outcomes across multiple datasets (TCGA, GSE79668 , GSE28735 , GSE57495 , ICGC, GSE62452 , GSE85916 , MTAB_6134, GSE71729 , GSE21501 ). (E) Kaplan‐Meier survival analyses for TNFAIP8 expression in PDAC cohorts. (TCGA, GSE85916 , GSE57495 ). Data were analyzed using the BEST (Biomarker Evaluation & Survival Tool) database (D, E). (F) IF images showing uptake of exosomes by CAFs. Scale bars, 20 µm. (G) ELISA quantification of TNFAIP8 levels in cell supernatants and exosomes from indicated PDAC cells (MIAPaCa‐2, PANC1) ( n = 3 biological replicates). (H) ELISA measurement of TNFAIP8 concentration in CM and exosome fractions collected from MIA PaCa‐2 cells under control or insulin treatment, with sh‐NC or sh‐TNFAIP8 expression. ( n = 3 biological replicates). (I) CCK‐8 assay for CAF viability after exosome or rTNFAIP8 treatment ( n = 3 biological replicates). (J) Representative EdU staining images and quantification of CAF proliferation under indicated treatments ( n = 5 biological replicates). Scale bars, 50 µm. (K) 3D fluorescence intensity plots showing α‐SMA and COL1A1 expression in CAFs under indicated treatments. (L) Multiplex IF staining of human PDAC tissues showing co‐localization of TNFAIP8 with α‐SMA and CK19, Samples include normal pancreas, Tumor‐INS‐Low, and Tumor‐INS‐High groups. The Tumor‐INS‐High group consists of PDAC patients with elevated insulin levels in both tumor tissue and matched fasting serum, whereas Tumor‐INS‐Low represents patients with lower insulin levels. (TMA, n = 60; Tumor‐INS‐High, n = 15; Tumor‐INS‐Low, n = 45). Scale bars: 500 and 50 µm. (M) Correlation analyses between TNFAIP8 expression and stromal markers (ACTA2 and COL1A1) in TCGA PDAC samples. Statistical comparisons between two groups were performed using a two‐tailed unpaired Student's t ‐tests (C). Data in (G, H, I, J) are shown as mean ± SD, analyzed by one‐way ANOVA with Tukey's test; Significance thresholds: ns, not significant; * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Article Snippet: The proliferation of PANC‐1 and MiaPaca‐2 cells was studied using the cell counting kit‐8 (CCK‐8, Dojindo, Japan) and 5‐ethynyl‐2′‐deoxyuridine assay (EdU, Beyotime, China) assays, as described in our previous studies [ ].

Techniques: Activation Assay, Control, Expressing, Biomarker Discovery, Enzyme-linked Immunosorbent Assay, Concentration Assay, CCK-8 Assay, Staining, Fluorescence, Multiplex Assay, Two Tailed Test

Journal: Signal Transduction and Targeted Therapy

Article Title: Glycolytic heterogeneity drives metabolic-targeted therapy in pancreatic ductal adenocarcinoma

doi: 10.1038/s41392-025-02546-8

Figure Lengend Snippet: Glycolytic Profiling and LDHA Inhibition Reveal Differential Sensitivity Across PDAC Cell Lines. a Heatmap of glycolytic signature expression, reported as normalized transcript per million (nTPM) across five PDAC cell lines from Human Protein Atlas. b Western blot analysis of LDHA expression in PL45, SW1990, PANC-1, MIAPaCa-2, and HPAF-II cells. c Glycolytic activity in PL45, SW1990, PANC-1, MIAPaCa-2, and HPAF-II cells after LDHA-i treatment, measured as extracellular acidification rate (ECAR). Each dot represents a biological replicate ( n = 6 per group). Data are represented as mean ± SD. Statistical analysis performed with a paired t -test. d Viability assay in MIAPaCa-2 (green), PANC-1 (blue), PL45 (purple), HPAF-II (red), and HPDE6c7 (brown) cells upon LDHA-i treatment at 24 and 48 h. Boxplots display IC50 values for each time point across cell lines, with statistical significance assessed by paired t -test ( n = 2 per group). On the right, GR50 and GRmax values represent drug potency and efficacy, respectively

Article Snippet: The PL45 (CRL-2558), SW1990 (CRL-2172), PANC-1 (CRL-1469), HPAF-II (CRL-1997), and MIAPaCa-2 (CRL-1420) cell lines were purchased from ATCC.

Techniques: Inhibition, Expressing, Western Blot, Activity Assay, Viability Assay

Journal: Signal Transduction and Targeted Therapy

Article Title: Glycolytic heterogeneity drives metabolic-targeted therapy in pancreatic ductal adenocarcinoma

doi: 10.1038/s41392-025-02546-8

Figure Lengend Snippet: Metabolomic, Proteomic, and Transcriptomic Profiling Uncovers the Impact of LDHA Inhibition in PDAC. a Amount of lactate in MIAPaCa-2 and PL45 cells at the basal level (gray) and after LDHA inhibition (blue). Each dot represents a biological replicate ( n = 6 per group). Data are shown as normalized intensity and are represented as mean ± SD. Statistical significance was calculated with a paired t -test. b Pathway enrichment analysis performed on metabolomics data in MIAPaCa-2 cells at basal level and after LDHA inhibition. The x -axis indicates pathway impact based on metabolite expression. The y -axis indicates p value transformed as −Log 10 . c Significant results from enrichment analysis performed on proteomics data in MIAPaCa-2 cells after LDHA inhibition. The x -axis indicates the normalized enrichment score. The label shows p value transformed as −Log 10 . d Enrichment plots for glycolysis and hypoxia in MIAPaCa-2 cells treated with LDHA-i. Normalized enrichment score and p value are reported in the figure. e Hallmarks significantly upregulated in PDAC patient samples exhibiting High glycolytic profile compared to those with Low glycolytic profile (left). Hallmarks significantly downregulated in MIAPaCa-2 cells following treatment with LDHA-i (right). The y -axis indicates the normalized enrichment score

Article Snippet: The PL45 (CRL-2558), SW1990 (CRL-2172), PANC-1 (CRL-1469), HPAF-II (CRL-1997), and MIAPaCa-2 (CRL-1420) cell lines were purchased from ATCC.

Techniques: Metabolomic, Inhibition, Expressing, Transformation Assay

Journal: Signal Transduction and Targeted Therapy

Article Title: Glycolytic heterogeneity drives metabolic-targeted therapy in pancreatic ductal adenocarcinoma

doi: 10.1038/s41392-025-02546-8

Figure Lengend Snippet: Integrative multiomics analysis correlates molecular signatures in PDAC. a Clustered image map of variables selected by multiblock partial least squares discriminant analysis (PLS-DA) based on omics datasets. Samples are displayed as rows, and selected features in columns. Histograms represent significant functional analysis results for proteins (light green), pathway analysis for metabolites (red), and enrichment analysis for lipids (purple). Statistical significance is expressed as −Log 10 transformed p values. b Circos plot from multiblock PLS-DA performed on proteomic (green), metabolomic (red), and lipidomic (purple) data in MIAPaCa-2 cells treated with LDHA-i. The plot shows correlations between 0.7 and −0.7 across proteins, metabolites, and lipids, represented on the side quadrants. The internal connecting lines show positive (light brown) and negative (black) correlations. c Network plot of correlated features derived by multiblock PLS-DA. Each node represents a variable, color-coded by type. The color of the edges indicates positive (light brown) or negative (black) correlations greater than ±0.7 between variables of different types

Article Snippet: The PL45 (CRL-2558), SW1990 (CRL-2172), PANC-1 (CRL-1469), HPAF-II (CRL-1997), and MIAPaCa-2 (CRL-1420) cell lines were purchased from ATCC.

Techniques: Functional Assay, Transformation Assay, Metabolomic, Derivative Assay