panc 1  (ATCC)

Journal: Materials Today Bio

Article Title: Stromal homeostasis-restoring “rocket-like” nanomedicine inhibited pancreatic tumor growth in vivo

doi: 10.1016/j.mtbio.2026.103014

Figure Lengend Snippet: In vitro evaluation of Panc-1 and Pan02 cells after different treatments. (A) Colony formation assay of Panc-1 and Pan02 cells after different treatments. (B) Quantification of colony numbers of Panc-1 and Pan02 cells under the indicated treatments. (C) Representative images of cell migration of Panc-1 and Pan02 cells after different treatments. (D) Quantification of residual area of Panc-1 and Pan02 cells in each group. (E) ROS fluorescence intensity of Panc-1 cells after different treatments. (F) ROS fluorescence intensity of Pan02 cells after different treatments. (G) Viability of Panc-1 cells co-cultured with L929 cells in a transwell system after different treatments. (H) Viability of Pan02 cells co-cultured with L929 cells in a transwell system after different treatments. (I) Representative CLSM images of Panc-1 cells co-stained with Calcein-AM (green) and PI (red) after treatment with different groups (scale bar: 200 μm). (J) Representative CLSM images of Pan02 cells co-stained with Calcein-AM (green) and PI (red) after treatment with different groups. (K) Immunofluorescence staining of uPA in Panc-1 cells after different treatments.(scale bar:100 μm). (L) Immunofluorescence staining of uPA in Pan02 cells after different treatments. Data are presented as mean ± standard deviation (SD), n = 3. Statistical significance was analyzed by one-way ANOVA with t -test; ns, not significant; ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

Article Snippet: Triethylamine (TEA, Sigma-Aldrich); Cetyltrimethylammonium bromide (CTAB, Xinyanbomei); Sodium salicylate (NaSal, Sigma-Aldrich); Tetraethyl orthosilicate (TEOS, CATO); 1,2-Bis(triethoxysilyl)ethane (BTES, Xinhengyan); Ethanol; Hydrochloric acid; Methanol; Gemcitabine (MedChemExpress); Ammonium bicarbonate (Coolaber); Urokinase-type plasminogen activator (Solarbio); CCK-8 kit (CWBIO); ROS staining kit (Poolyue); Calcein-AM/PI kit (DOJINDO); anti-uPA antibody (HUABIO); Calcium chloride (Supelco); Indocyanine green (zrbiorise); Dulbecco's modified Eagle medium (DMEM, Sigma-Aldrich); Panc-1, Pan02, and L929 cells (ATCC); Fluorescein isothiocyanate (FITC, Qisong); 4′,6-diamidino-2-phenylindole (DAPI, Solarbio); DUTP (Roche); IPR-803 (MCE).

Techniques: In Vitro, Colony Assay, Migration, Fluorescence, Cell Culture, Staining, Immunofluorescence, Standard Deviation

Journal: International Journal of Oncology

Article Title: Therapeutic implications of targeting cancer testis antigen MAGEA1 in cervical cancer

doi: 10.3892/ijo.2026.5870

Figure Lengend Snippet: Effects of MAGEA1 knockdown on mRNA/protein expression and cellular functions including proliferation, viability, migration, and invasion. (A) Western blotting detected MAGEA1 expression in SK-OV-3 (ovarian cancer), Panc1 (pancreatic cancer), HupT3 (pancreatic cancer), HeLa (cervical cancer), and T24 (urinary bladder carcinoma). GAPDH was used as a loading control. HeLa was transfected with shMAGEA1 #1 and #2 and shNC was established as a control. (B) Reverse transcription-quantitative PCR and (C) western blot analysis were used to estimate the efficiency of knockdown. (D) Cell viability was determined by MTT assay after 24 h of cell seeding. (E) A significant decrease in cell proliferation was observed in MAGEA1 knockdown compared with control. The number of proliferated cells is presented as a percentage of the control. (F) Representative images from wound scratch at different time points (magnification, ×40). (G) Percentages of wound closure at 24 and 72 h are shown as a bar graph. The scratched area and lines were quantified by ImageJ software with the MRI tool. (H) Cell migration and invasion were confirmed by Transwell migration and invasion assays. Representative images of cells are illustrated below. Scale bar, 500 μ m. (I) Quantification of migrated and invaded cells in distinct groups. The number of migrated and invaded cells is presented as a percentage of the control. Error bars represent the mean ± SEM. * P<0.05, ** P<0.01, *** P<0.005. MAGEA1, MAGE family member A1; sh, short hairpin; NC, negative control.

Article Snippet: HeLa (CCL-2) and Panc1 (CRL-1469) were purchased from American Type Culture Collection.

Techniques: Knockdown, Expressing, Migration, Western Blot, Control, Transfection, Reverse Transcription, Real-time Polymerase Chain Reaction, MTT Assay, Software, Negative Control

Journal: Journal of Cellular and Molecular Medicine

Article Title: EN2 Regulates Pancreatic Cancer Initiation, Progression, and Epithelial‐Mesenchymal Transition Through the Notch Signalling Pathway

doi: 10.1111/jcmm.71158

Figure Lengend Snippet: Expression of EN2 in human pancreatic cancer tissues. (A, B), Pancreatic Tissue Arrays containing normal and cancerous tissues were purchased from Biomax. EN2 expression was measured by IHC. Representative photographs of 60 pancreatic tissues from various stages of pancreatic cancer. Blue = nuclei, Brown/pink colour = EN2. * = significantly different from normal, p = < 0.01. (C) TCGA data on the expression of EN2 mRNA. * = significantly different from normal.

Article Snippet: Human pancreatic cancer cell lines (PANC‐1 and AsPC‐1) and human normal pancreatic ductal epithelial cells (HPNE) were purchased from the American Type Culture Collection (ATCC, Manassas, VA).

Techniques: Expressing

Journal: Journal of Cellular and Molecular Medicine

Article Title: EN2 Regulates Pancreatic Cancer Initiation, Progression, and Epithelial‐Mesenchymal Transition Through the Notch Signalling Pathway

doi: 10.1111/jcmm.71158

Figure Lengend Snippet: The expression of EN2 in HPNE, pancreatic cancer cell lines, and pancreatic CSCs. (A), Protein expression of EN2 in HPNE, pancreatic cancer cell lines, and pancreatic CSCs. Crude proteins were isolated, and EN2 expression was measured by Western blot analysis. β‐Actin was used as a loading control. (B), Expression of EN2 mRNA in HPNE, pancreatic cancer cell lines, and pancreatic CSCs. RNA was isolated, and EN2 expression was measured by q‐RT‐PCR. GAPDH was used as an internal control. Data represent mean ( n = 4) ± SD. *, # and % = significantly different from HPNE ( p < 0.05). (C), Expression of EN2. Immunocytochemistry was performed to examine EN2 expression in HPNE, PANC‐1, and AsPC‐1 cells.

Article Snippet: Human pancreatic cancer cell lines (PANC‐1 and AsPC‐1) and human normal pancreatic ductal epithelial cells (HPNE) were purchased from the American Type Culture Collection (ATCC, Manassas, VA).

Techniques: Expressing, Isolation, Western Blot, Control, Reverse Transcription Polymerase Chain Reaction, Immunocytochemistry

Journal: Journal of Cellular and Molecular Medicine

Article Title: EN2 Regulates Pancreatic Cancer Initiation, Progression, and Epithelial‐Mesenchymal Transition Through the Notch Signalling Pathway

doi: 10.1111/jcmm.71158

Figure Lengend Snippet: EN2 knockdown reduces motility, migration, invasion, and EMT marker expression in pancreatic cancer cells. (A) Cell Motility Assay. Pancreatic cancer cells expressing scrambled or EN2 shRNA were cultured in petri dishes. After 18 h, a linear scratch was generated using a fine pipette tip, and phase‐contrast images were captured at 0 and 48 h to assess wound closure. (B) Cell Migration Assay. Cells expressing scrambled or EN2 shRNA were seeded in six‐well plates, and migration was quantified as described in the Materials and Methods. Data represent mean ( n = 4) ± SD. * p < 0.05 compared with the scrambled control. (C) Cell Invasion Assay. Cells expressing scrambled or EN2 shRNA were seeded in six‐well plates, and invasion was measured as described in the Materials and Methods. Data represent mean ( n = 4) ± SD. * p < 0.05 compared with the scrambled control. (D, E) Total RNA was isolated, and the expression of E‐cadherin, N‐cadherin, Snail, Slug, and Zeb1 was quantified by qRT‐PCR. GAPDH served as the internal control. Data represent mean ( n = 4) ± SD. * p < 0.05 between groups.

Article Snippet: Human pancreatic cancer cell lines (PANC‐1 and AsPC‐1) and human normal pancreatic ductal epithelial cells (HPNE) were purchased from the American Type Culture Collection (ATCC, Manassas, VA).

Techniques: Knockdown, Migration, Marker, Expressing, Motility Assay, shRNA, Cell Culture, Generated, Transferring, Cell Migration Assay, Control, Invasion Assay, Isolation, Quantitative RT-PCR

Journal: Journal of Cellular and Molecular Medicine

Article Title: EN2 Regulates Pancreatic Cancer Initiation, Progression, and Epithelial‐Mesenchymal Transition Through the Notch Signalling Pathway

doi: 10.1111/jcmm.71158

Figure Lengend Snippet: EN2 shRNA inhibits Notch‐target genes and Nanog expression and RBP JK transcription in pancreatic cancer cells. (A, B), Expression of Notch target genes. RNA was isolated, and the expression of cMyc, Cyclin D1, Bcl‐2, Hes 1 and Nanog was measured in cells by q‐RT‐PCR. GAPDH was used as an internal control. Data represent mean ( n = 4) ± SD. * = significantly different between groups ( p < 0.05). (C), RBP JK transcription. PANC‐1 and AsPC‐1 cells were transduced with RBP JK ‐responsive GFP/firefly luciferase viral particles (pGreen Fire1‐ RBP JK with EF1, System Biosciences) along with EN2/scrambled or EN2 shRNA viral particles. RBP JK reporter activity was measured as we described . Data represent mean ( n = 4) ± SD. * = significantly different from scrambled control group ( p < 0.05).

Article Snippet: Human pancreatic cancer cell lines (PANC‐1 and AsPC‐1) and human normal pancreatic ductal epithelial cells (HPNE) were purchased from the American Type Culture Collection (ATCC, Manassas, VA).

Techniques: shRNA, Expressing, Isolation, Reverse Transcription Polymerase Chain Reaction, Control, Transduction, Luciferase, Activity Assay

Journal: Mediators of Inflammation

Article Title: The Vitamin D3 Analog Calcipotriol Attenuates Pancreatic Cancer Malignancy via Downregulating Thrombospondin 1 in Pancreatic Stellate Cells

doi: 10.1155/mi/2632235

Figure Lengend Snippet: Effects of Cal on aPSC activation. (A) (Left) VDR mRNA expression in PDAC cell lines (AsPC‐1, MIA PaCa‐2, and PANC‐1) and aPSCs was determined by qRT‐PCR ( n = 3). (Right) CYP24A1 mRNA expression in PDAC or aPSCs treated with DMSO or Cal (100 nM and 48 h) was examined by qRT‐PCR ( n = 3). (B) VDR protein expression in PDAC cell lines (AsPC‐1, MIA PaCa‐2, and PANC‐1) and aPSCs was determined by western blot ( n = 3). (C) Correlation analysis between α‐SMA and VDR mRNA expression in aPSCs, with GAPDH normalization ( n = 9). (D) VDR and α‐SMA gene expression in aPSCs treated with DMSO or Cal (100 nM and 48 h) was evaluated by qRT‐PCR ( n = 3). (E) VDR and α‐SMA protein expression in aPSCs treated with DMSO or Cal (100 nM and 48 h) ( n = 4). (F) Immunocytochemistry showing α‐SMA expression in aPSCs treated with DMSO or Cal (100 nM and 48 hr) ( n = 3). (G) EZ4U assay indicating the impacts of Cal on the proliferation of aPSCs ( n = 3). (H) Transwell migration assay and (I) wound healing showing the effects of Cal on aPSCs’ migration ability ( n = 3). caPSCs, PSCs derived from pancreatic cancer; cpPSCs, PSCs derived from chronic pancreatitis; cuPSCs, culture‐activated PSCs derived from normal tissue; aPSCs, activated PSCs; HPF, high‐power field; Ctr, control group treated with DMSO. All experiments were conducted in triplicate. ns, not significant. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001.

Article Snippet: Human PDAC cell lines PANC‐1 (male, American Type Culture Collection [ATCC] CRL‐1469, RRID: CVCL_0480), MIA PaCa‐2 (male, ATCC CRL‐1420, RRID: CVCL_0428), and AsPC‐1 (female, ATCC CRL‐1682, RRID: CVCL_0152) were purchased directly from the ATCC (Manassas, VA, USA) in 2015.

Techniques: Activation Assay, Expressing, Quantitative RT-PCR, Western Blot, Gene Expression, Immunocytochemistry, Transwell Migration Assay, Migration, Derivative Assay, Control

Journal: Mediators of Inflammation

Article Title: The Vitamin D3 Analog Calcipotriol Attenuates Pancreatic Cancer Malignancy via Downregulating Thrombospondin 1 in Pancreatic Stellate Cells

doi: 10.1155/mi/2632235

Figure Lengend Snippet: Dose‐dependent effect of rTHBS1 on PDAC malignancy. (A) Transwell migration assays showing the response of PDAC cell lines PANC‐1 and MIA PaCa‐2 to varying concentrations of rTHBS1 (0, 0.5, and 5 μg/mL). (B) Transwell invasion assays were used to quantify the invasive potential of the same PDAC cell lines under the same rTHBS1 treatments. (C) Proliferation of PDAC cells was assessed by EZ4U assay after treatment with rTHBS1 at 0, 0.5, 5, and 20 μg/mL. (D) Wound healing assays complement the migration analysis, with images and quantification of the migration area closure. (E) Representative micrographs depicting morphological alterations in PANC‐1 and MIA PaCa‐2 cells when cultured in standard medium, aPSCs‐CM, and standard medium supplemented with 5 μg/mL of rTHBS1. All experiments were conducted in triplicate. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.

Article Snippet: Human PDAC cell lines PANC‐1 (male, American Type Culture Collection [ATCC] CRL‐1469, RRID: CVCL_0480), MIA PaCa‐2 (male, ATCC CRL‐1420, RRID: CVCL_0428), and AsPC‐1 (female, ATCC CRL‐1682, RRID: CVCL_0152) were purchased directly from the ATCC (Manassas, VA, USA) in 2015.

Techniques: Migration, Cell Culture

Journal: Mediators of Inflammation

Article Title: The Vitamin D3 Analog Calcipotriol Attenuates Pancreatic Cancer Malignancy via Downregulating Thrombospondin 1 in Pancreatic Stellate Cells

doi: 10.1155/mi/2632235

Figure Lengend Snippet: Inhibition of aPSCs‐CM–driven malignancy in PDAC by THBS1 neutralizing antibody. THBS1 neutralizing Ab diminished aPSCs‐CM–induced migration (A, C, D), invasion (B), proliferation (E–F), and EMT (G–H) of PDAC but had no effects on Cal‐aPSCs‐CM–induced malignancy of PDAC. aPSCs‐CM, CM from aPSCs pretreated with DMSO; Cal‐aPSCs‐CM, CM harvested from aPSCs pretreated with 100 nM Cal for 48 h. CM was then pretreated with 1 μg/mL of THBS1 Ab or control IgG and added to the PDAC. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.

Article Snippet: Human PDAC cell lines PANC‐1 (male, American Type Culture Collection [ATCC] CRL‐1469, RRID: CVCL_0480), MIA PaCa‐2 (male, ATCC CRL‐1420, RRID: CVCL_0428), and AsPC‐1 (female, ATCC CRL‐1682, RRID: CVCL_0152) were purchased directly from the ATCC (Manassas, VA, USA) in 2015.

Techniques: Inhibition, Migration, Control

Journal: Mediators of Inflammation

Article Title: The Vitamin D3 Analog Calcipotriol Attenuates Pancreatic Cancer Malignancy via Downregulating Thrombospondin 1 in Pancreatic Stellate Cells

doi: 10.1155/mi/2632235

Figure Lengend Snippet: Attenuation of aPSCs‐CM–induced PDAC aggressiveness by CD47 blockade. CD47 blocking Ab diminished aPSCs‐CM–induced migration (A, C, D), invasion (B), proliferation (E–F), and EMT (G–H) of PDAC but had no effects on Cal‐aPSCs‐CM–induced aggressiveness of PDAC. PDAC were pretreated with 2 μg/mL CD47 blocking Ab or control IgG. All experiments were conducted in triplicate. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.

Article Snippet: Human PDAC cell lines PANC‐1 (male, American Type Culture Collection [ATCC] CRL‐1469, RRID: CVCL_0480), MIA PaCa‐2 (male, ATCC CRL‐1420, RRID: CVCL_0428), and AsPC‐1 (female, ATCC CRL‐1682, RRID: CVCL_0152) were purchased directly from the ATCC (Manassas, VA, USA) in 2015.

Techniques: Blocking Assay, Migration, Control

Journal: Mediators of Inflammation

Article Title: The Vitamin D3 Analog Calcipotriol Attenuates Pancreatic Cancer Malignancy via Downregulating Thrombospondin 1 in Pancreatic Stellate Cells

doi: 10.1155/mi/2632235

Figure Lengend Snippet: Differential impact on PDAC organoid morphology and EMT marker expression by aPSCs‐CM and antibody interventions. (A) Representative bright‐field images displaying PDAC organoids over 5 days in control (aPSCs‐CM), treated with Cal‐aPSCs‐CM, with THBS1 antibody‐depleted aPSCs‐CM, and with organoids where CD47 has been blocked, followed by treatment with aPSCs‐CM. (B) Western blot analysis of E‐cadherin and vimentin in organoids subjected to these varied treatments. (C) Protein expression quantification normalized to GAPDH, demonstrating the effect of THBS1 depletion and CD47 inhibition on EMT markers in PDAC organoids. All experiments were conducted in triplicate. ∗ p < 0.05 and ∗∗ p < 0.01. Scale bar: 100 μm.

Article Snippet: Human PDAC cell lines PANC‐1 (male, American Type Culture Collection [ATCC] CRL‐1469, RRID: CVCL_0480), MIA PaCa‐2 (male, ATCC CRL‐1420, RRID: CVCL_0428), and AsPC‐1 (female, ATCC CRL‐1682, RRID: CVCL_0152) were purchased directly from the ATCC (Manassas, VA, USA) in 2015.

Techniques: Marker, Expressing, Control, Western Blot, Inhibition

Journal: Small Science

Article Title: Ultrastructural Study of Microphysiological Systems of the Tumor Microenvironment

doi: 10.1002/smsc.202500567

Figure Lengend Snippet: Schematic overview of the study workflow. The MPS consisted of one‐chamber microfluidic devices used to generate two cancer‐on‐a‐chip models: PDAC and LAC. Cells were embedded in natural hydrogels composed of egg white (EW)‐gelatin and collagen type I, respectively. At the end of the culture period, devices were fixed, stained, dehydrated, disassembled, critically point‐dried, mounted, and coated for SEM and FIB‐SEM imaging. For LAC models, the FIB was additionally used to prepare thin lamellae for TEM. This workflow enabled high‐resolution observation of both external and internal organization of 3D multicellular structures, including cell–cell and cell–matrix interactions, matrix deposition, and intercellular communication.

Article Snippet: Human PDAC cell line PANC‐1, and human LAC cell line A549 from the American Type Culture Collection (ATCC, USA) were used for this work.

Techniques: Staining, Imaging

Journal: Small Science

Article Title: Ultrastructural Study of Microphysiological Systems of the Tumor Microenvironment

doi: 10.1002/smsc.202500567

Figure Lengend Snippet: Schematic of a generic MPS used in this study. The inner geometry consists of a single microfluidic channel with ports for hydrogel loading and perfusion of culture medium. The central chamber contains the 3D multicellular tumor culture embedded in a hydrogel matrix. Two distinct cancer‐on‐a‐chip models were implemented, each in a separate device: pancreatic ductal adenocarcinoma (PDAC, PANC‐1 cells) and lung adenocarcinoma (LAC, A549 cells). This schematic highlights the overall architecture of the chip and the spatial arrangement of the tumor constructs, hydrogel, and medium channels.

Article Snippet: Human PDAC cell line PANC‐1, and human LAC cell line A549 from the American Type Culture Collection (ATCC, USA) were used for this work.

Techniques: Construct

Journal: Small Science

Article Title: Ultrastructural Study of Microphysiological Systems of the Tumor Microenvironment

doi: 10.1002/smsc.202500567

Figure Lengend Snippet: (A) Scheme of the MPS of the TME of PDAC, consisting of a hydrogel‐based cancer‐on‐a‐chip model where the PANC‐1 cell line was used. (B) Brightfield microscopy representative images of the PANC‐1 aggregates grown over 14 days of culture in EW/gelatin hydrogels. Zoomed area shows single aggregate. Dual beam FIB‐SEM representative image of EW/gelatin hydrogel after 14 days of culture, displaying the typical nanoglobular morphology of these hydrogels. (C) Dual beam FIB‐SEM representative images of the surface of PANC‐1 aggregates in EW/gelatin hydrogel. ECM: extracellular matrix produced by the cells. Orange asterisk: EW/gelatin hydrogel. Green arrows: unions between cells. Orange arrows: unions between the cells and the hydrogel. Yellow arrows: spherical particles. Blue arrows: large spherical particles.

Article Snippet: Human PDAC cell line PANC‐1, and human LAC cell line A549 from the American Type Culture Collection (ATCC, USA) were used for this work.

Techniques: Microscopy, Produced

Journal: Small Science

Article Title: Ultrastructural Study of Microphysiological Systems of the Tumor Microenvironment

doi: 10.1002/smsc.202500567

Figure Lengend Snippet: (A) Dual beam FIB‐SEM representative images of the ECM secreted by the PANC‐1 cells. Image iii shows some measurements of the diameter of the fibers that comprise the ECM. (B) Measurements of the diameter and length of the ECM fibers secreted by the PANC‐1 cells. Data shown in violin plot as its distribution with median and the interquartile range (IQR), each dot represent a measurement ( n = 98 for fiber diameter and n = 46 for fiber length).

Article Snippet: Human PDAC cell line PANC‐1, and human LAC cell line A549 from the American Type Culture Collection (ATCC, USA) were used for this work.

Techniques:

Journal: Small Science

Article Title: Ultrastructural Study of Microphysiological Systems of the Tumor Microenvironment

doi: 10.1002/smsc.202500567

Figure Lengend Snippet: (A) Dual beam FIB‐SEM representative images of the internal cell organization of the aggregates formed by PANC‐1 cells in EW/gelatin hydrogels. Image i shows the surface of the aggregate milled with the ion beam along the yellow line. Images ii–v show internal sections of the aggregate shown in image i. Image vi belongs to a different aggregate. Individual cells are indicated by red numbers. For additional guidance to identify cell boundaries, Figure S1 provides the same images with a colored overlay mask highlighting the cellular regions. Light blue arrows: darker and denser intracellular areas. Green arrows: membrane projections connecting adjacent cells. Yellow arrows: EVs secreted by the cells. (B) Measurements of the size (i.e., diameter) of the EVs secreted by the PANC‐1 cells. Data shown in violin plot as its distribution with median and the IQR, each dot represents a measurement ( n = 48).

Article Snippet: Human PDAC cell line PANC‐1, and human LAC cell line A549 from the American Type Culture Collection (ATCC, USA) were used for this work.

Techniques: Membrane