Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

Article Title: Co-treatment of ticagrelor and anti-PD-1 immunotherapy in tumor-associated macrophages reduces pancreatic cancer cell growth and migration through the TGF-β1/Smad2 pathway

doi: 10.1016/j.biopha.2025.118695

Figure Lengend Snippet: TAMs in the PDAC TME express PD-1. The pancreatic tissue slides from healthy and pancreatic cancer patients were immunostained with (A) anti-PD-L1 and (B) anti-PD-1 and anti-CD163 (a marker for TAMs). In human pancreatic cancer specimens, PD-L1 was expressed, and PD-1 was co-localized with CD163. The images are representative of three independent experiments. Scale bar: 20μm. 40 × magnification.

Article Snippet: Patient-derived human pancreatic cancer cells (HPCCs, 77007–07, Celprogen) were cultured in a human pancreatic cancer cell line complete medium.

Techniques: Marker

Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

Article Title: Co-treatment of ticagrelor and anti-PD-1 immunotherapy in tumor-associated macrophages reduces pancreatic cancer cell growth and migration through the TGF-β1/Smad2 pathway

doi: 10.1016/j.biopha.2025.118695

Figure Lengend Snippet: Co-treatment of ticagrelor and cemiplimab synergistically increases TAM’s phagocytic ability and decreases the migration of patient-derived human pancreatic cancer cells. THP-1 cells were cultured with PMA (10 ng/mL) for 24 h to differentiate into macrophages (M0). Following 24 h of resting, cells were incubated with 30 % v/v of conditioned media from human pancreatic cancer cells (HPCCs) for 48 h (H-TAMs). (A) The expressions of TAM markers, CD206, CD163, PD-1, and Arg1, and CD163 + PD-1 + were detected using flow cytometry, N = 3. (B) A phagocytosis assay was performed to determine the phagocytic ability of H-TAMs, as described above. Representative images of H-TAM phagocytosis are shown (scale bar: 75μm). (C) Phagocytosis is expressed as a percentage of tumor cells phagocytosed by TAMs (white arrow) per field of view normalized to the untreated co-culture group set to 100 %. N = 3, *P ≤ 0.05, **P ≤ 0.01, ****P ≤ 0.0001. (D) HPCCs were seeded in the upper chamber of the Transwell co-culture system (8 μm pore size), while H-TAMs were placed in the lower chamber. The H-TAMs were treated with 2 μM ticagrelor, 2 μM cemiplimab, or 2 μM ticagrelor and 2 μM cemiplimab. After 48 h of incubation, the migrated cells were fixed and stained. Representative images of migrated HPCCs are shown (scale bar: 250μm). (E) Data was quantified as the number of migrated cells normalized to the untreated cancer cell group set to 100 %. N = 3–4, **P ≤ 0.01, ****P ≤ 0.0001.

Article Snippet: Patient-derived human pancreatic cancer cells (HPCCs, 77007–07, Celprogen) were cultured in a human pancreatic cancer cell line complete medium.

Techniques: Migration, Derivative Assay, Cell Culture, Incubation, Flow Cytometry, Phagocytosis Assay, Co-Culture Assay, Pore Size, Staining

Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

Article Title: Co-treatment of ticagrelor and anti-PD-1 immunotherapy in tumor-associated macrophages reduces pancreatic cancer cell growth and migration through the TGF-β1/Smad2 pathway

doi: 10.1016/j.biopha.2025.118695

Figure Lengend Snippet: (A) The concentration of TGF-β1 was measured in plasma samples from healthy donors and cancer patients by Multi-Species TGF-β 3-Plex Discovery Assay ® . N = 5, *P ≤ 0.05. (B) The lysates prepared from the pancreatic tissue samples from healthy donors and cancer patients were used to perform a Western blot to detect the level of phosphorylated Smad2. Western blotting images are shown. (C) Data was quantified as the ratio of phosphorylated Smad2 to β-actin. N = 3–4, **P ≤ 0.01.

Article Snippet: Patient-derived human pancreatic cancer cells (HPCCs, 77007–07, Celprogen) were cultured in a human pancreatic cancer cell line complete medium.

Techniques: Concentration Assay, Clinical Proteomics, Western Blot

Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

Article Title: Co-treatment of ticagrelor and anti-PD-1 immunotherapy in tumor-associated macrophages reduces pancreatic cancer cell growth and migration through the TGF-β1/Smad2 pathway

doi: 10.1016/j.biopha.2025.118695

Figure Lengend Snippet: The inhibitory effect of the co-treatment of ticagrelor and cemiplimab on TAM-induced migration of human pancreatic cancer cells is reversed by exogenous TGF-β1. Transwell assay was performed to determine the migration capacity of HPCCs as described above. The H-TAMs were treated with 2 μM ticagrelor, 2 μM cemiplimab, 2 μM ticagrelor and 2 μM cemiplimab, or 5 ng/mL exogenous TGF-β1 and the co-treatment for 48 h. (A) Representative images of migrated HPCCs are shown (scale bar: 250 μm). (B) Data was quantified as the number of migrated cells normalized to the untreated cancer cell group set to 100 %. N = 3–4, *P ≤ 0.05, ***P ≤ 0.001, ****P ≤ 0.0001.

Article Snippet: Patient-derived human pancreatic cancer cells (HPCCs, 77007–07, Celprogen) were cultured in a human pancreatic cancer cell line complete medium.

Techniques: Migration, Transwell Assay

Journal: Colloids and surfaces. B, Biointerfaces

Article Title: Peptide-targeted, stimuli-responsive polymersomes for delivering a cancer stemness inhibitor to cancer stem cell microtumors.

doi: 10.1016/j.colsurfb.2017.12.036

Figure Lengend Snippet: Fig. 5. Cellular uptake studies in monolayer and microtumor cultures of prostate and pancreatic cancer stem cells. Panels (A–F): prostate cancer stem cells (scale bar: 25 m), and

Article Snippet: Prostate cancer stem cells were maintained in human prostate cancer stem cell complete growth media with serum and antibiotics and pancreatic cancer stem cell were maintained in human pancreatic cancer stem cell complete growth media with serum and antibiotics from Celprogen.

Techniques:

Journal: Colloids and surfaces. B, Biointerfaces

Article Title: Peptide-targeted, stimuli-responsive polymersomes for delivering a cancer stemness inhibitor to cancer stem cell microtumors.

doi: 10.1016/j.colsurfb.2017.12.036

Figure Lengend Snippet: Fig. 6. Expression of neuropilin-1 in prostate and pancreatic cancer stem cells as determined

Article Snippet: Prostate cancer stem cells were maintained in human prostate cancer stem cell complete growth media with serum and antibiotics and pancreatic cancer stem cell were maintained in human pancreatic cancer stem cell complete growth media with serum and antibiotics from Celprogen.

Techniques: Expressing

Journal: Colloids and surfaces. B, Biointerfaces

Article Title: Peptide-targeted, stimuli-responsive polymersomes for delivering a cancer stemness inhibitor to cancer stem cell microtumors.

doi: 10.1016/j.colsurfb.2017.12.036

Figure Lengend Snippet: Fig. 7. The viability of prostate and pancreatic cancer stem cells in monolayer and spheroid cultures. (A) Monolayer cultures of prostate cancer stem cells, (B) monolayer cultures

Article Snippet: Prostate cancer stem cells were maintained in human prostate cancer stem cell complete growth media with serum and antibiotics and pancreatic cancer stem cell were maintained in human pancreatic cancer stem cell complete growth media with serum and antibiotics from Celprogen.

Techniques:

Journal: Colloids and surfaces. B, Biointerfaces

Article Title: Peptide-targeted, stimuli-responsive polymersomes for delivering a cancer stemness inhibitor to cancer stem cell microtumors.

doi: 10.1016/j.colsurfb.2017.12.036

Figure Lengend Snippet: Fig. 9. Flow cytometry analysis of the effect of napabucasin on prostate (A) and pancreatic cancer stem cells (B) with Annexin V and PI staining.

Article Snippet: Prostate cancer stem cells were maintained in human prostate cancer stem cell complete growth media with serum and antibiotics and pancreatic cancer stem cell were maintained in human pancreatic cancer stem cell complete growth media with serum and antibiotics from Celprogen.

Techniques: Flow Cytometry, Staining

Journal: Journal of materials chemistry. B

Article Title: Design and evaluation of nanoscale materials with programmed responsivity towards epigenetic enzymes.

doi: 10.1039/d4tb00514g

Figure Lengend Snippet: Fig. 6 Interaction of the block copolymers and HDAC8-responsive nanoparticles with different types of PDAC cells and non-cancerous HPNE cells in vitro. (A) PEG-block-poly(acetylated L-lysine) block copolymers studied in this work do not trigger cytotoxicity in different cell lines. (B) Chemical structure of the STAT3 inhibitor, Napabucasin (NAPA), which has been used as the model hydrophobic drug to demonstrate the encapsulation and HDAC-mediated release activity of the nanoparticles in the context of drug delivery. (C) HDAC 8 (1 mM) triggers the release of NAPA, and over 90% of the encapsulated drug is released from these nanoparticles after incubation with the enzyme for 3 h. The standard deviation of mean is taken for N = 3 replicates. Without the enzyme, the drug release rate and extent were significantly decreased. (D) NAPA-loaded nanoparticles showed a concentration- dependent effect on different types of cancer cells, with a more prominent effect on cancer stem cells (CSCs).

Article Snippet: The fourth cell variant is patient-derived xenograft pancreatic cancer stem cells (CSCs) obtained from Celprogen.

Techniques: Blocking Assay, In Vitro, Encapsulation, Activity Assay, Incubation, Standard Deviation, Concentration Assay

Journal: Oncology Letters

Article Title: Anticancer effect of arsenite on cell migration, cell cycle and apoptosis in human pancreatic cancer cells

doi: 10.3892/ol.2016.4564

Figure Lengend Snippet: Effects of PDGF-BB on the migration of AsPC-1 and BxPC-3 pancreatic cancer cells, compared with normal PE cells. (A) AsPC-1, (B) BxPC-3 and (C) PE cells (5×104 cells/well) were treated with the indicated doses of arsenite for 24 h, prior to be seeded in the upper Boyden chamber. Following incubation for 16 h, cells were exposed to 30 ng/ml PDGF-BB for 36 h at 37°C. Cells were then fixed, stained and visualized under a microscope. The average number of migrated cells from five randomly selected fields on the lower surface of the membrane was counted. Data were obtained from ≥3 independent experiments. *P<0.05 vs. controls. Right panels show representative images of the migrated cells stained with clonogenic reagent. PDGF, platelet-derived growth factor; PE, pancreatic epithelial.

Article Snippet: Primary normal human pancreatic epithelial (PE) cells were purchased from DS Pharma Biomedical Co., Ltd. (Osaka, Japan) and maintained in CSC medium (Cell Systems Corporation, Kirkland, WA, USA).

Techniques: Migration, Incubation, Staining, Microscopy, Membrane, Derivative Assay

Journal: Oncology Letters

Article Title: Anticancer effect of arsenite on cell migration, cell cycle and apoptosis in human pancreatic cancer cells

doi: 10.3892/ol.2016.4564

Figure Lengend Snippet: Effects of arsenite on PARP cleavage in AsPC-1, BxPC-3 and PE cells. (A) AsPC-1, (B) BxPC-3 and (C) PE cells were exposed to arsenite (30 µM) for the indicated time periods. Protein extracts were then harvested and examined by western blotting using anti-PARP and anti-glyceraldehyde-3-phosphate dehydrogenase antibodies. Background-subtracted signal intensity of each protein band was normalized to GAPDH. Data are presented as the mean ± standard deviation of triplicate assay. *P<0.05. PARP, poly(adenosine diphosphate-ribose) polymerase; PE, pancreatic epithelial; GAPDH, glyceraldehyde-3-phosphate dehydrogenase.

Article Snippet: Primary normal human pancreatic epithelial (PE) cells were purchased from DS Pharma Biomedical Co., Ltd. (Osaka, Japan) and maintained in CSC medium (Cell Systems Corporation, Kirkland, WA, USA).

Techniques: Western Blot, Standard Deviation

Journal: Oncology Letters

Article Title: Anticancer effect of arsenite on cell migration, cell cycle and apoptosis in human pancreatic cancer cells

doi: 10.3892/ol.2016.4564

Figure Lengend Snippet: Effects of arsenite on the phosphorylation of p44/p42 MAPK and Akt in AsPC-1, BxPC-3 and PE cells. (A) AsPC-1, (B) BxPC-3 and (C) PE cells were exposed to arsenite (30 µM) and incubated with 30 ng/ml platelet-derived growth factor-BB for the indicated time periods. Protein extracts were then harvested and examined by western blotting using specific antibodies against phospho-p44/p42 MAPK, p44/p42 MAPK, phospho-Akt and Akt. Background-subtracted signal intensity of each protein band was normalized to Akt. Data are presented as the mean ± standard deviation of triplicate assay. *P<0.05 vs. cells without arsenite exposure. PE, pancreatic epithelial; PDGF, platelet-derived growth factor; phospho, phosphorylated; MAPK, mitogen-activated protein kinase; M, marker.

Article Snippet: Primary normal human pancreatic epithelial (PE) cells were purchased from DS Pharma Biomedical Co., Ltd. (Osaka, Japan) and maintained in CSC medium (Cell Systems Corporation, Kirkland, WA, USA).

Techniques: Phospho-proteomics, Incubation, Derivative Assay, Western Blot, Standard Deviation, Marker