Journal: Cell Communication and Signaling : CCS

Article Title: Transcriptional deregulation by FOXM1–JUP signaling confers dual oncogenic drivers for pancreatic tumorigenesis and therapeutic resistance

doi: 10.1186/s12964-025-02512-5

Figure Lengend Snippet: FOXM1 transcriptionally regulates JUP in PDAC. A , IHC: Levels of JUP and FOXM1 protein expression in PDAC ( A1 ). Linear regression analysis: the correlation of FOXM1 and JUP ( n = 16) ( A2 ). Correlation analysis of FOXM1 and JUP expression in PDAC ( http://gepia.cancer-pku.cn/ ) ( n = 329) ( A3 ). B-C , Expression of FOXM1 was altered by transfection with siRNA or expression vectors. The impact of FOXM1 on JUP expression in PDAC cells by WB ( B ) and RT-qPCR ( C ) analyses. Note that FOXM1 inhibited the expression of JUP mRNA and protein in AsPC-1 and PL45, while the overexpression of FOXM1 increased the JUP mRNA and protein in AsPC-1 and PL45. FOXM1 regulated the expression of both JUP protein and mRNA. D , Direct binding of JUP to FOXM1 promoter. Sequences and positions of putative FOXM1-binding elements on JUP promoter (#1 and #2) ( D1 ). Normal IgG was used as a control, and 1.5% of the total cell lysates was subjected to PCR before immunoprecipitation. The ChIP assay to test the direct binding of FOXM1 on the genomic locus of JUP promoter regions ( D2 ). Quantitative analysis of ChIP results ( D3 ). All data are expressed as mean ± SD, n = 3. Statistical analysis: student t-test or ANOVA, * P < 0.05, ** P < 0.01 and *** P < 0.001 vs. control group

Article Snippet: To investigate the relationship between JUP expression and chemotherapy resistance, we used gemcitabine (GEM) and oxaliplatin (OXA) (MedChemExpress, USA), commonly used drugs for PDAC chemotherapy.

Techniques: Expressing, Transfection, Quantitative RT-PCR, Over Expression, Binding Assay, Control, Immunoprecipitation

Journal: Cell Communication and Signaling : CCS

Article Title: Transcriptional deregulation by FOXM1–JUP signaling confers dual oncogenic drivers for pancreatic tumorigenesis and therapeutic resistance

doi: 10.1186/s12964-025-02512-5

Figure Lengend Snippet: FOXM1-mediated cancer cell proliferation requires JUP expression. A - C , FOXM1-silenced and JUP-overexpressing PDAC cells were established. The protein levels of FOXM1 and JUP were determined by Western blot ( A1 ) and the mRNA levels by RT-qPCR ( A2 ); cell viability by CCK-8 ( B ), and colony formation assay and the number of clones by ImageJ software. Note that JUP mediated FOXM1-induced PDAC cell proliferation and colony formation ( C ). D , PDAC cells were injected subcutaneously into mice. Tumor sizes were measured weekly ( D1 ). The mice were sacrificed and the tumors were removed and weighed ( D2 , D3 ). All data were expressed as mean ± SD, n = 3. Statistical analysis: student t-test or ANOVA, * P < 0.05, ** P < 0.01 and *** P < 0.001 vs. control group

Article Snippet: To investigate the relationship between JUP expression and chemotherapy resistance, we used gemcitabine (GEM) and oxaliplatin (OXA) (MedChemExpress, USA), commonly used drugs for PDAC chemotherapy.

Techniques: Expressing, Western Blot, Quantitative RT-PCR, CCK-8 Assay, Colony Assay, Clone Assay, Software, Injection, Control

Journal: Cell Communication and Signaling : CCS

Article Title: Transcriptional deregulation by FOXM1–JUP signaling confers dual oncogenic drivers for pancreatic tumorigenesis and therapeutic resistance

doi: 10.1186/s12964-025-02512-5

Figure Lengend Snippet: FOXM1-mediated therapeutic resistance requires JUP expression. AsPC-1, PL45 and Panc02 cells were either transfection with siRNA (NC or siJUP) or expression vectors (p3.1 or pJUP) to alter the expression levels of JUP. A , The cells were then treated in vitro with different concentrations of GEM and OXA for 48 h and cell viability was determined by CCK8 assay. Note that increased expression of JUP significantly enhanced PDAC cells resistance to both GEM and OXA, whereas reduced expression of JUP did the opposite. B , GEM/OXA in vivo treatment model scheme. C , D , The cells with altered expression of JUP were subcutaneously injected into groups of mice, which then received treatment of drugs ( C , GEM; D , OXA) for indicated times. The tumor growth curves ( C1 , D1 ), subcutaneous tumors from mice ( C2 , D2 ) and tumor weights ( C3 , D3 ) were shown. Note that increased JUP expression significantly reduced the therapeutic efficacy of both GEM and OXA. All data were expressed as mean ± SD, n = 5. Statistical analysis: student t-test or ANOVA, * P < 0.05, ** P < 0.01 and *** P < 0.001 vs. control group

Article Snippet: To investigate the relationship between JUP expression and chemotherapy resistance, we used gemcitabine (GEM) and oxaliplatin (OXA) (MedChemExpress, USA), commonly used drugs for PDAC chemotherapy.

Techniques: Expressing, Transfection, In Vitro, CCK-8 Assay, In Vivo, Injection, Drug discovery, Control

Journal: Oncology reports

Article Title: Zoledronic acid inhibits proliferation of human fibrosarcoma cells with induction of apoptosis, and shows combined effects with other anticancer agents.

doi: 10.3892/or_00000851

Figure Lengend Snippet: Figure 5. Growth inhibitory effects of concurrent treatment with ZOL and anticancer agents on human fibrosarcoma cell lines. The capacity of ZOL and several antitumor agents to inhibit the growth of HT1080 cells was determined by employing the trypan blue dye exclusion method. Data from three independent experiments were collected, and Student's t-test was used to evaluate the efficacy of concurrent treatment with ZOL and other agents and to compare the effects of each anticancer agent alone. P-values of <0.05 were considered statistically significant and derived from two-sided statistical tests. X-axis: a, control; b, 1.2 μM of ZOL alone; c, 0.5xIC50 of antitumor drug alone; d, combination of b with c; e, 1.0xIC50 of antitumor drug; f, combination of b with d. Y-axis is cell counts (x105). (A) doxorubicin; (B) cisplatin; (C) etoposide; (D) 5-fluorouracil; (E) docetaxel; (F) paclitaxel; (G) gemcitabine; (H) methotrexate.

Article Snippet: Doxorubicin (from Toronto Research Chemicals, Inc., Toronto, Canada), 5-fluorouracil (from Nacalai Tesque, Inc., Kyoto, Japan), cisplatin, paclitaxel, docetaxel, gemcitabine (from LKT laboratories, Inc., St. Paul, MN, USA), etoposide (from CalbiochemNovabiochem, Cor(Merck KGaA), Darmstadt, Germany), and methotrexate (from Sigma Aldrich, Tokyo, Japan) were purchased from commercial sources.

Techniques: Derivative Assay, Control

Journal: PLoS ONE

Article Title: 3D collagen fibrillar microstructure guides pancreatic cancer cell phenotype and serves as a critical design parameter for phenotypic models of EMT

doi: 10.1371/journal.pone.0188870

Figure Lengend Snippet: (A) Table summarizing pancreatic cell line phenotype, patient derivation, and relevant mutations . (B) BxPC-3, Panc-1,and MiaPaCa-2 cells were cultured on 2D plastic (4x10 3 cells/well) for 4 days, stained for actin (green), vimentin (red), E-cadherin (yellow), and nuclei (blue), and imaged using confocal microscopy. Images represent z-stack projections (20 μm thickness; scale bar = 30 μm). (C) Gemcitabine IC50 values (mean ± SD) were determined from 10-point dose response curves for cell lines cultured on 2D plastic. Letters indicate statistically different groups (p<0.05, n = 5).

Article Snippet: PDAC cell sensitivity to gemcitabine (Santa Cruz Biotechnology, Dallas, TX) was determined by dosing with a 10-point drug dilution (1:5 dilution starting at 200 μM) and calculating IC50 values from data obtained with Alamar Blue metabolic indicator (Invitrogen, Frederick, MD).

Techniques: Cell Culture, Staining, Confocal Microscopy

Journal: PLoS ONE

Article Title: 3D collagen fibrillar microstructure guides pancreatic cancer cell phenotype and serves as a critical design parameter for phenotypic models of EMT

doi: 10.1371/journal.pone.0188870

Figure Lengend Snippet: (A) Table and (B) graph summarizing gemcitabine IC50 values (mean ± SD) for PDAC lines cultured (2x10 5 cells/mL) for 4 days within Oligomer (0.9 mg/mL, 100 Pa) or Matrigel (100 Pa). Asterisk (*) indicates statistically different groups (p<0.05, N = 3–4, n = 3).

Article Snippet: PDAC cell sensitivity to gemcitabine (Santa Cruz Biotechnology, Dallas, TX) was determined by dosing with a 10-point drug dilution (1:5 dilution starting at 200 μM) and calculating IC50 values from data obtained with Alamar Blue metabolic indicator (Invitrogen, Frederick, MD).

Techniques: Cell Culture

Journal: PLoS ONE

Article Title: 3D collagen fibrillar microstructure guides pancreatic cancer cell phenotype and serves as a critical design parameter for phenotypic models of EMT

doi: 10.1371/journal.pone.0188870

Figure Lengend Snippet: (A) Gemcitabine IC50 values (mean ± SD; n = 3) and (B) S-phase fraction (mean ± SD; N = 2, n = 3) for BxPC-3 and MiaPaCa-2 cells cultured for 4 days within 3D Oligomer (2x10 5 cells/mL) prepared at stiffness values of 100 Pa (0.9 mg/mL), 500 Pa (2 mg/mL), and 1000 Pa (3 mg/mL). Asterisk (*) indicates statistically different groups (p<0.05); note that values between different cell types were not compared.

Article Snippet: PDAC cell sensitivity to gemcitabine (Santa Cruz Biotechnology, Dallas, TX) was determined by dosing with a 10-point drug dilution (1:5 dilution starting at 200 μM) and calculating IC50 values from data obtained with Alamar Blue metabolic indicator (Invitrogen, Frederick, MD).

Techniques: Cell Culture

Journal: Journal of controlled release : official journal of the Controlled Release Society

Article Title: R11 modified tumor cell membrane nanovesicle-camouflaged nanoparticles with enhanced targeting and mucus-penetrating efficiency for intravesical chemotherapy for bladder cancer.

doi: 10.1016/j.jconrel.2022.09.055

Figure Lengend Snippet: Fig. 1. Hendeca-arginine peptide (R11) was polymerized with DNA to form nanocomplexes, which enabled one-step surface-functionalization of tumor cell membrane with large amounts of R11 at the extracellular side of cell membrane. The tumor cell membrane fragments with the R11 shell were used to encapsule gemcitabine-loaded PLGA nanoparticles by extrusion to construct a dual-targeting and mucus-penetrating drug delivery system for intravesical chemotherapy in bladder cancer.

Article Snippet: Gemcitabine elaidate was purchased from MedChemExpress.

Techniques: Membrane, Construct

Journal: Cell Reports Medicine

Article Title: CAN-Scan: A multi-omic phenotype-driven precision oncology platform identifies prognostic biomarkers of therapy response for colorectal cancer

doi: 10.1016/j.xcrm.2025.102053

Figure Lengend Snippet:

Article Snippet: Gemcitabine , MedChemExpress , Cat# HY-17026.

Techniques: Recombinant, Red Blood Cell Lysis, Sequencing, Software, RNA sequencing

Journal: Journal of proteomics

Article Title: Quantitative proteomics of the yeast Hsp70/Hsp90 interactomes during DNA damage reveal chaperone-dependent regulation of ribonucleotide reductase.

doi: 10.1016/j.jprot.2014.09.028

Figure Lengend Snippet: Fig. 7 – Ribonucleotide reductase is a client of Hsp70 and Hsp90 in human breast cancer cells. (A) MCF-7 human breast cancer cells were transiently transfected with no DNA (control) or plasmids expressing SBP-tagged Hsp70 or Hsp90. After 48 h recovery in media, cells were lysed and pull-down was performed with streptavidin-conjugated magnetic beads. Captured proteins were separated by SDS-PAGE, transferred and probed with streptavidin-HRP or anti-hRRM2 antibody and secondary antibody HRP conjugate. (B) MCF-7 cells grown to 50% confluence were treated either with DMSO, Hsp70 inhibitor VER-155008, or Hsp90 inhibitor 17-AAG for 48 h. Cells were lysed and hRRM2 levels were determined by Western blot with anti-hRRM2 antibody. Equal loading was determined using anti-tubulin immunoreactivity. (C) MCF-7 cells were incubated without chaperone inhibitors or with subtoxic concentrations of VER-155008 to inhibit Hsp70 or 17-AAG to inhibit Hsp90. After 24 h, gemcitabine was added at the indicated concentrations. After another 24 h, cell death was determined by Trypan Blue dye exclusion assay. Data shown are mean ± SEM of three replicates (*P < 0.05 compared to no chaperone inhibitor, t-test).

Article Snippet: 17-N-allylamino-17-demethoxygeldanamycin (17-AAG), VER-155008 and gemcitabine hydrochloride were purchased from Tocris Bioscience.

Techniques: Transfection, Control, Expressing, Magnetic Beads, SDS Page, Western Blot, Incubation, Exclusion Assay