Journal: Cancers

Article Title: Externally Applied Electromagnetic Fields and Hyperthermia Irreversibly Damage Cancer Cells

doi: 10.3390/cancers15133413

Figure Lengend Snippet: Effect of EMFs and HT on cancer cell viability. ( A ) Effect of EMFs. Cancer cells were seeded and 24 h later exposed to EMFs (100–500 kHz × 1–5 h). Control values (0 kHz) were 1.14 ± 0.03 A2058, 1.13 ± 0.04 AsPC1, and 1.20 ± 0.05 MDA-MB-231 (×10 6 ) viable cells ( n = 5 in all cases). * p < 0.05 comparing all conditions versus controls (0 kHz) ( n = 5 t -test). ( B ) Effect of HT. Cancer cells were seeded and 24 h later exposed to HT (42–52 °C × 20–40 min). * p < 0.05 ** p < 0.01 comparing all conditions versus controls (37 °C) ++ p < 0.01 comparing 40 min versus 20 min ( n = 5 t test). ( C ) Effect of EMFS and HT. Cancer cells were seeded and 24 h later exposed to EMFs (100 kHz × 4 h) and HT (52 °C × 40 min from min 120 to min 160 of the 4 h period where cells were constantly exposed to the EMFs). The surviving cells were cultured for 24 additional hours without further exposure to EMFs and HT. A two-way analysis of variance (ANOVA) was used to make comparisons among the different groups after 4 h of treatment with EMFs + HT and 24 h after. Different letters indicate differences p < 0.05 ( n = 5).

Article Snippet: Human AsPC1/Luciferase Stable Cells were obtained from GenTarget Inc. (San Diego, CA, USA).

Techniques: Control, Cell Culture

Journal: Cancers

Article Title: Externally Applied Electromagnetic Fields and Hyperthermia Irreversibly Damage Cancer Cells

doi: 10.3390/cancers15133413

Figure Lengend Snippet: Effect of EMFs and HT on ROS generation and the molecular mechanisms of apoptosis.

Article Snippet: Human AsPC1/Luciferase Stable Cells were obtained from GenTarget Inc. (San Diego, CA, USA).

Techniques:

Journal: Cancers

Article Title: Externally Applied Electromagnetic Fields and Hyperthermia Irreversibly Damage Cancer Cells

doi: 10.3390/cancers15133413

Figure Lengend Snippet: Effect of EMFs + HIFU-induced HT, gemcitabine and/or PT on the growth of AsPC1 pancreas carcinoma. Cancer cells were inoculated subcutaneously on day 0, and mice were treated with EMFs and HIFU as described under Materials and Methods. ( A ) EMFs and HIFU were applied once per day per three consecutive days (Monday to Wednesday) for two consecutive weeks starting on day 14 after tumor inoculation. Gemcitabine (50 mg/kg) was administered twice on days 14 and 21. A one-way analysis of variance (ANOVA) was used to make comparisons among the different experimental groups at each time point. Different letters indicate statistical differences p < 0.05 ( n = 15 mice per experimental group). ( B ) A disodium salt of PT phosphate (Chromadex Inc. Los Angeles CA) (100 mg of PT/kg) was administered i.p. (one dose 30 min before starting each irradiation session with EMFs and HT). A one-way analysis of variance (ANOVA) was used to make comparisons among the different experimental groups. Different letters indicate statistical differences p < 0.05 ( n = 12 mice per experimental group). ( C ) Representative images of mice inoculated with AsPC1/Luciferase Stable Cells and treated with EMFs HT and gemcitabine (GEM) or EMFs HT gemcitabine and PT.

Article Snippet: Human AsPC1/Luciferase Stable Cells were obtained from GenTarget Inc. (San Diego, CA, USA).

Techniques: Irradiation, Luciferase

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

Article Title: Systemic administration of human mesenchymal stromal cells infected with polymer-coated oncolytic adenovirus induces efficient pancreatic tumor homing and infiltration

doi: 10.1016/j.jconrel.2019.04.040

Figure Lengend Snippet: Cancer cell killing effect and viral replication of oAd/RLX-PCDP complex-loaded hMSCs on various pancreatic cancer cells. (A) Oncolytic effect by PBS, naked oAd/RLX, oAd/RLX-loaded hMSCs, or oAd/RLX-PCDP-loaded hMSCs. Cells (AsPC-1, PANC-1, and MIA PaCa-2) were infected with naked oAd/RLX, oAd/RLX-loaded or oAd/RLX-PCDP-loaded hMSCs at various MOIs. After 4 (AsPC-1 and PANC-1) or 6 (MIA PaCa-2) days post-infection, cell viability was measured by MTT assay. For oAd/RLX groups, the cell viability solely accounts for the absorbance readout of respective cancer cell types. For oAd/RLX- and oAd/RLX-PCDP-loaded hMSC groups, the total cell viability (as determined by absorbance readout) accounts for both respective types of pancreatic cancer cells and surviving hMSC carrier. (B) Viral production. Cells (AsPC-1, PANC-1, and MIA PaCa-2) were infected with naked oAd/RLX, oAd/RLX-loaded hMSCs, or oAd/RLX-PCDP-loaded hMSCs. At 72 h post-infection, viral genomic copies were measured by real-time quantitative PCR. Results represent the mean ± SD of triplicate experiments. ***P < 0.001 versus oAd/RLX-loaded hMSC control.

Article Snippet: In vivo antitumor efficacy Pancreatic cancer xenograft model was established by injecting 5 × 10 6 AsPC-1 cells into the subcutaneous of 6 weeks-old female nude mice (n=8) (Charles River Inc., Wilmington, MA).

Techniques: Infection, MTT Assay, Real-time Polymerase Chain Reaction

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

Article Title: Systemic administration of human mesenchymal stromal cells infected with polymer-coated oncolytic adenovirus induces efficient pancreatic tumor homing and infiltration

doi: 10.1016/j.jconrel.2019.04.040

Figure Lengend Snippet: Tumor-tropic migratory properties of oAd/RLX-PCDP complex-loaded hMSCs. oAd/RLX, oAd/RLX-PEI, and oAd/RLX-PCDP complex were treated into hMSCs at 5 MOI. After 18 h, these cells were detached and co-cultured with pancreatic cancer cells (AsPC-1) into the transwell plate for 30 h. Then, the migrated cells were fixed and stained with hematoxylin and eosin solution. All conditions were done in quadruplicate and repeated in two separate experiments. ***P < 0.001 versus uninfected hMSC (negative control) or naked oAd/RLX.

Article Snippet: In vivo antitumor efficacy Pancreatic cancer xenograft model was established by injecting 5 × 10 6 AsPC-1 cells into the subcutaneous of 6 weeks-old female nude mice (n=8) (Charles River Inc., Wilmington, MA).

Techniques: Cell Culture, Staining, Negative Control

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

Article Title: Systemic administration of human mesenchymal stromal cells infected with polymer-coated oncolytic adenovirus induces efficient pancreatic tumor homing and infiltration

doi: 10.1016/j.jconrel.2019.04.040

Figure Lengend Snippet: In vivo antitumor efficacy of oAd/RLX-PCDP-loaded hMSCs in tumor-bearing mice. Pancreatic tumor xenograft model was established by injecting AsPC-1 cells (5 × 106) subcutaneously in nude mice (n=8). Following the confirmation of tumorigenesis, the treatments were systemically administered on 4 day intervals for total of 3 injections when the average tumor volumes reached 90 mm3. (A) Relative tumor volume of each treatment group at day 21 post treatment in respect to initial tumor volume from day 1. (B) Relative body weight of each treatment group in respect to PBS treatment group at 21 days post initial treatment. (C) Histological and immunohistochemical analysis of tumor tissues from mice treated with PBS, PCDP, hMSC, naked oAd/RLX, oAd/RLX-loaded hMSC, or oAd/RLX-PCDP-loaded hMSC. Tumor tissues were collected from mice at 3 days after the final treatment. Representative sections were stained with H & E or MT solution. TUNEL assay was performed to detect apoptosis, and the expression of E1A was assessed by immunohistochemistry. Data presented as mean ± SD. ***P < 0.001 versus PBS, PCDP, hMSC, naked oAd/RLX, and oAd/RLX-loaded hMSC.

Article Snippet: In vivo antitumor efficacy Pancreatic cancer xenograft model was established by injecting 5 × 10 6 AsPC-1 cells into the subcutaneous of 6 weeks-old female nude mice (n=8) (Charles River Inc., Wilmington, MA).

Techniques: In Vivo, Immunohistochemical staining, Staining, TUNEL Assay, Expressing, Immunohistochemistry

Journal: International Journal of Surgery (London, England)

Article Title: Single dual-specific anti-PD-L1/TGF-β antibody synergizes with chemotherapy as neoadjuvant treatment for pancreatic ductal adenocarcinoma: a preclinical experimental study

doi: 10.1097/JS9.0000000000001226

Figure Lengend Snippet: Antitumor activity of BiTP combinatorial chemotherapy in orthotopic PDAC models. (A) Treatment plan and schedules. (B) Schematic diagram of the KPC model. The approximate time frame of mouse tumor progression to borderline resectable (BR), locally advanced (LA), and terminal (TERM) are days 7, 14, and 21, respectively. (C) Representative tumor images of orthotopic PDAC mice receiving different therapies. (D) Tumor weights and volumes on day 30. (E) The table included the survival rate (%), tumor proliferation (T/C, %), tumor growth inhibition (TGI, %), and resectability status of orthotopic PDAC mice receiving different therapies on day 30, and the median survival time (MST) in survival assays. (F) Kaplan–Meier plot survival curve and pairwise comparison results of orthotopic PDAC mice receiving different therapies in survival assays. Data presented in the graphs represent mean±standard deviation (SD) (**** P <0.0001; *** P <0.001; ** P <0.01; * P <0.05; ns P >0.05). BiTP, anti-PD-L1/TGF-β antibody; CTH, chemotherapy; PDAC, pancreatic ductal adenocarcinoma; PD-L1, programmed cell death 1 ligand 1.

Article Snippet: Human PDAC cell lines ASPC-1 (with Kras G12D mutation) and CFPAC-1 (with Kras G12V mutation) and human pancreatic ductal epithelial cell line HPDE6-C7 were obtained from China Center for the Conservation of Typical Cultures (CCTCC).

Techniques: Activity Assay, Inhibition, Comparison, Standard Deviation

Journal: International Journal of Surgery (London, England)

Article Title: Single dual-specific anti-PD-L1/TGF-β antibody synergizes with chemotherapy as neoadjuvant treatment for pancreatic ductal adenocarcinoma: a preclinical experimental study

doi: 10.1097/JS9.0000000000001226

Figure Lengend Snippet: Decisions about resectability status in PDAC murine models.

Article Snippet: Human PDAC cell lines ASPC-1 (with Kras G12D mutation) and CFPAC-1 (with Kras G12V mutation) and human pancreatic ductal epithelial cell line HPDE6-C7 were obtained from China Center for the Conservation of Typical Cultures (CCTCC).

Techniques: Membrane

Journal: International Journal of Surgery (London, England)

Article Title: Single dual-specific anti-PD-L1/TGF-β antibody synergizes with chemotherapy as neoadjuvant treatment for pancreatic ductal adenocarcinoma: a preclinical experimental study

doi: 10.1097/JS9.0000000000001226

Figure Lengend Snippet: Preclinical assessment of neoadjuvant BiTP combinatorial chemotherapy for the treatment of PDAC. (A) Treatment plan and schematic diagram of treatment schedules. (B) Schematic diagram of distal pancreatectomy in orthotopic PDAC mice model. (C) Representative images of tumors. (D) Tumor weights and volumes of direct surgery (day 7) and post-neoadjuvant therapy resections (day 24). (E) Table of resectability status (day 24), operative mortality (OM), and median survival time (MST) of orthotopic PDAC mice receiving different therapies. (F–H) Kaplan–Meier plot survival curve and pairwise comparison results of orthotopic PDAC mice receiving different therapies in survival assays. Data presented in the graphs represent mean±standard deviation (SD). (**** P <0.0001; *** P <0.001; ** P <0.01; * P <0.05; ns P >0.05). AC, adjuvant chemotherapy; ACI, adjuvant chemo-immunotherapy; BiTP, anti-PD-L1/TGF-β antibody; CTH, chemotherapy; NAC, neo-adjuvant chemotherapy; NACI, neo-adjuvant chemo-immunotherapy; NAT, neo-adjuvant therapy; SRG, surgery.

Article Snippet: Human PDAC cell lines ASPC-1 (with Kras G12D mutation) and CFPAC-1 (with Kras G12V mutation) and human pancreatic ductal epithelial cell line HPDE6-C7 were obtained from China Center for the Conservation of Typical Cultures (CCTCC).

Techniques: Comparison, Standard Deviation, Adjuvant

Journal: International Journal of Surgery (London, England)

Article Title: Single dual-specific anti-PD-L1/TGF-β antibody synergizes with chemotherapy as neoadjuvant treatment for pancreatic ductal adenocarcinoma: a preclinical experimental study

doi: 10.1097/JS9.0000000000001226

Figure Lengend Snippet: BiTP reverses TGF-β-induced EMT (epithelial–mesenchymal transition) of PDAC (pancreatic ductal adenocarcinoma) cells. (A) CCK-8 (Cell Counting Kit-8) assay to measure the effect of BiTP on TGF-β-mediated chemoresistance in PDAC cells. After 10 ng/ml TGF-β1, 10 5 pM BiTP or hIgG treatment for 24 h. HPDE6-C7, CFPAC-1, ASPC-1, and KPC cells growing in 96-well plates were exposed to serial dilutions of gemcitabine and nab-paclitaxel for 72 h and CCK-8 assays was performed. (B) The representative images of IHC (immunohistochemistry) staining of Ki67 in orthotopic PDAC mice model and statistical graph of the percentage of Ki67-positive cells. (C) The representative images of TUNEL staining for apoptosis (green) and nuclei (DAPI, blue) in orthotopic PDAC mice model and statistical graph of the percentage of apoptosis cells. (D) Transwell assays to measure the effect of BiTP on TGF-β-mediated migration and in PDAC cells. After 10 ng/ml TGF-β1, 10 5 pM BiTP or hIgG treatment for 96 h. 1×10 4 CFPAC-1 and KPC cells were seeded in the upper chambers and Transwell assays were performed. (E) Western blotting assays exploring the chemotherapy-induced EMT and the blocking effect of BiTP. (F) The representative images of IHC staining of E-cadherin in orthotopic PDAC mice model. Statistical graph of the AOD (average optical density) of E-cadherin. (G) The representative images of IF staining of Vimentin (green) and α-SMA (rose red) in orthotopic PDAC mice model. Statistical graph of the arbitrary units of Vimentin and α-SMA. (H) The representative images of Masson staining in orthotopic PDAC mice model. Statistical graph of the percentage of collagen volume fraction (%). Data presented in the graphs represent mean±standard deviation (SD). (**** P <0.0001; *** P <0.001; ** P <0.01; * P <0.05; ns P >0.05). BiTP, anti-PD-L1/TGF-β antibody; CTH, chemotherapy; KPC, LSL-Kras(+/G12D);LSL-Trp53(+/R172H);Pdx1-Cre; PDAC, pancreatic ductal adenocarcinoma; PD-L1, programmed cell death 1 ligand 1; TGF-β, transforming growth factor-β.

Article Snippet: Human PDAC cell lines ASPC-1 (with Kras G12D mutation) and CFPAC-1 (with Kras G12V mutation) and human pancreatic ductal epithelial cell line HPDE6-C7 were obtained from China Center for the Conservation of Typical Cultures (CCTCC).

Techniques: CCK-8 Assay, Cell Counting, Immunohistochemistry, Staining, TUNEL Assay, Migration, Western Blot, Blocking Assay, Standard Deviation

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: METTL3-dependent m6A methylation of circCEACAM5 fuels pancreatic cancer progression through DKC1 activation

doi: 10.1007/s00018-025-05653-5

Figure Lengend Snippet: Upregulation of circCEACAM5 in pancreatic cancer tissues and cell lines. A RT‒qPCR analysis of circCEACAM5 expression in pancreatic cancer tissues and adjacent normal tissues ( n = 32 per group). B RT‒qPCR analysis of circCEACAM5 expression in pancreatic cancer cell lines and normal ductal epithelial cells (HPDE-C7). The data are presented as the means ± SDs from three independent experiments. ** p < 0.01, *** p < 0.001 compared with adjacent normal tissues or HPDE-C7 cells, respectively. Student’s t test or one-way ANOVA was used for statistical analysis

Article Snippet: Our study utilized four human pancreatic cancer cell lines (BxPC-3, MIA-PaCa-2, AsPC-1, and PANC-1) and human pancreatic ductal epithelial (HPDE) cells, all of which were derived from Procell (Wuhan, China).

Techniques: Expressing

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: METTL3-dependent m6A methylation of circCEACAM5 fuels pancreatic cancer progression through DKC1 activation

doi: 10.1007/s00018-025-05653-5

Figure Lengend Snippet: circCEACAM5 enhances proliferation, invasion, and migration while suppressing apoptosis in pancreatic cancer cells. A RT‒qPCR analysis of circCEACAM5 expression in AsPC-1 cells following circCEACAM5 overexpression or knockdown. B CCK-8 assay of AsPC-1 cell proliferation. C EdU incorporation assay. Scale bar = 100 μm. D , E Transwell migration and invasion assays. Scale bar = 50 μm. F Flow cytometry analysis of apoptosis. The data are presented as the means ± SDs from three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001 compared with the respective controls. One-way ANOVA was used for statistical analysis

Article Snippet: Our study utilized four human pancreatic cancer cell lines (BxPC-3, MIA-PaCa-2, AsPC-1, and PANC-1) and human pancreatic ductal epithelial (HPDE) cells, all of which were derived from Procell (Wuhan, China).

Techniques: Migration, Expressing, Over Expression, Knockdown, CCK-8 Assay, Flow Cytometry

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: METTL3-dependent m6A methylation of circCEACAM5 fuels pancreatic cancer progression through DKC1 activation

doi: 10.1007/s00018-025-05653-5

Figure Lengend Snippet: circCEACAM5 promotes pancreatic tumor growth and inhibits apoptosis in vivo. A RT‒qPCR analysis of circCEACAM5 expression in xenograft tumors. B Tumor volume measurements over time. C H&E staining of tumor sections. Scale bar = 100 μm. D , E Ki-67 and TUNEL staining of tumor sections. Scale bar = 100 μm. The data are presented as the means ± SDs ( n = 5 mice per group). ** p < 0.01, *** p < 0.001 compared with the respective controls. One-way ANOVA was used for statistical analysis

Article Snippet: Our study utilized four human pancreatic cancer cell lines (BxPC-3, MIA-PaCa-2, AsPC-1, and PANC-1) and human pancreatic ductal epithelial (HPDE) cells, all of which were derived from Procell (Wuhan, China).

Techniques: In Vivo, Expressing, Staining, TUNEL Assay

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: METTL3-dependent m6A methylation of circCEACAM5 fuels pancreatic cancer progression through DKC1 activation

doi: 10.1007/s00018-025-05653-5

Figure Lengend Snippet: METTL3-mediated m6A modification regulates circCEACAM5 expression in pancreatic cancer. A Predicted m6A modification sites in circCEACAM5. B , C RT‒qPCR analysis of METTL3 expression in pancreatic cancer tissues and cell lines. D m6A-specific immunoprecipitation of circCEACAM5 in AsPC-1 cells. E m6A-specific immunoprecipitation of circCEACAM5 following METTL3 knockdown. F RNA pull-down assay showing that circCEACAM5 binds to METTL3. G RT‒qPCR analysis of circCEACAM5 expression following METTL3 modulation. The data are presented as the means ± SDs from three independent experiments. ** p < 0.01, *** p < 0.001 compared with the respective controls. Student’s t test or one-way ANOVA was used for statistical analysis

Article Snippet: Our study utilized four human pancreatic cancer cell lines (BxPC-3, MIA-PaCa-2, AsPC-1, and PANC-1) and human pancreatic ductal epithelial (HPDE) cells, all of which were derived from Procell (Wuhan, China).

Techniques: Modification, Expressing, Immunoprecipitation, Knockdown, Pull Down Assay

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: METTL3-dependent m6A methylation of circCEACAM5 fuels pancreatic cancer progression through DKC1 activation

doi: 10.1007/s00018-025-05653-5

Figure Lengend Snippet: METTL3 promotes aggressive phenotypes in pancreatic cancer cells. A Western blot analysis of METTL3 protein levels following overexpression or knockdown. B CCK-8 assay of AsPC-1 cell proliferation. C EdU incorporation assay. Scale bar = 100 μm. D Transwell migration and invasion assays. Scale bar = 50 μm. E Flow cytometry analysis of apoptosis. The data are presented as the means ± SDs from three independent experiments. ** p < 0.01, *** p < 0.001 compared with the respective controls. One-way ANOVA was used for statistical analysis

Article Snippet: Our study utilized four human pancreatic cancer cell lines (BxPC-3, MIA-PaCa-2, AsPC-1, and PANC-1) and human pancreatic ductal epithelial (HPDE) cells, all of which were derived from Procell (Wuhan, China).

Techniques: Western Blot, Over Expression, Knockdown, CCK-8 Assay, Migration, Flow Cytometry

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: METTL3-dependent m6A methylation of circCEACAM5 fuels pancreatic cancer progression through DKC1 activation

doi: 10.1007/s00018-025-05653-5

Figure Lengend Snippet: circCEACAM5 specifically interacts with DKC1 in pancreatic cancer cells. A Predicted RNA-binding proteins (RBPs) for circCEACAM5 via starBase2. B , C RNA pull-down assays showing the associations of DKC1 and UPF1 with circCEACAM5. D RIP assay detecting circCEACAM5 enrichment via anti-DKC1 or IgG antibodies. E Western blot analysis of DKC1 protein levels following circCEACAM5 knockdown. The data are presented as the means ± SDs from three independent experiments. ** p < 0.01 compared with the IgG control. Student’s t test was used for statistical analysis

Article Snippet: Our study utilized four human pancreatic cancer cell lines (BxPC-3, MIA-PaCa-2, AsPC-1, and PANC-1) and human pancreatic ductal epithelial (HPDE) cells, all of which were derived from Procell (Wuhan, China).

Techniques: RNA Binding Assay, Western Blot, Knockdown, Control

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: METTL3-dependent m6A methylation of circCEACAM5 fuels pancreatic cancer progression through DKC1 activation

doi: 10.1007/s00018-025-05653-5

Figure Lengend Snippet: DKC1 mediates the oncogenic effects of circCEACAM5 in pancreatic cancer cells. A Western blot analysis of DKC1 protein levels following DKC1 overexpression. B CCK-8 assay of AsPC-1 cell proliferation. C , D Transwell migration and invasion assays. Scale bar = 50 μm. E Flow cytometry analysis of apoptosis. The data are presented as the means ± SDs from three independent experiments. ** p < 0.01, *** p < 0.001 compared with the indicated groups. One-way ANOVA was used for statistical analysis

Article Snippet: Our study utilized four human pancreatic cancer cell lines (BxPC-3, MIA-PaCa-2, AsPC-1, and PANC-1) and human pancreatic ductal epithelial (HPDE) cells, all of which were derived from Procell (Wuhan, China).

Techniques: Western Blot, Over Expression, CCK-8 Assay, Migration, Flow Cytometry