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ATCC human pdac cell lines panc 1

Effects of Cal on aPSC activation. (A) (Left) VDR mRNA expression in <t>PDAC</t> cell lines (AsPC‐1, MIA PaCa‐2, and <t>PANC‐1)</t> 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.

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1) Product Images from "The Vitamin D3 Analog Calcipotriol Attenuates Pancreatic Cancer Malignancy via Downregulating Thrombospondin 1 in Pancreatic Stellate Cells"

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

Journal: Mediators of Inflammation

doi: 10.1155/mi/2632235

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.

Figure Legend 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.

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

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.

Figure Legend 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.

Techniques Used: Migration, Cell Culture

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.

Figure Legend 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.

Techniques Used: Inhibition, Migration, Control

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.

Figure Legend 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.

Techniques Used: Blocking Assay, Migration, Control

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.

Figure Legend 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.

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

Image Search Results

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.

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.

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.

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.

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

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.

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

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.

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

(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.

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

(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).

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:

(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).

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

Radiation fails to enhance macrophage phagocytosis despite inducing immunogenic signals. A, Schematic illustration of scRNA-seq in animal models. t-SNE, t-distributed stochastic neighbor embedding. B, scRNA-seq analysis of immunogenic markers on tumor cells from control (Ctrl) or irradiated LLC tumors ( n = 3). C and D, Flow cytometry histograms and mean fluorescence intensity (MFI) of CRT on control or irradiated H460 ( C ) and PANC-1 ( D ) cells ( n = 3). Normalized to the control group. E, Immunofluorescence images of CRT (red) on control or irradiated H460 cells. F, Flow cytometry histograms and mean fluorescence intensity of tumor cells CRT from control or irradiated KPC tumor models ( n = 6). Normalized to the control group. G and H, Culture medium HMGB1 levels from control or irradiated H460 ( G ) and PANC-1 ( H ) cells measured by ELISA ( n = 3). I and J, Extracellular ATP release from control or irradiated H460 ( I ) and PANC-1 ( J ) cells measured by ELISA ( n = 3). K, scRNA-seq–derived M1 signature scores of tumor-associated macrophages from irradiated or control LLC tumors ( n = 3). L, Flow cytometry histograms and quantitation of control or irradiated H460 cell phagocytosis by THP-1 macrophages ( n = 3). M, Immunofluorescence images and quantitation of control or irradiated H460 cell (green) phagocytosis by THP-1 macrophages (red), with arrows indicating phagocytic events ( n = 6). Scale bars, 50 μm. N, Flow cytometry dotplot and quantitation of tumor cell phagocytosis by tumor-associated macrophages from control or irradiated LLC tumor ( n = 6). IR, 8 Gy irradiation. All data are presented as mean ± SEM and compared using a two-tailed Student t test. NS, not significant. A, Created in BioRender. Kong, L. (2026) https://BioRender.com/rwdzfwn .

Journal: Cancer Research

Article Title: Radiation-Enhanced CD24 Membrane Trafficking via GPI Anchoring Mediates Antitumor Immune Evasion

doi: 10.1158/0008-5472.CAN-25-2616

Figure Lengend Snippet: Radiation fails to enhance macrophage phagocytosis despite inducing immunogenic signals. A, Schematic illustration of scRNA-seq in animal models. t-SNE, t-distributed stochastic neighbor embedding. B, scRNA-seq analysis of immunogenic markers on tumor cells from control (Ctrl) or irradiated LLC tumors ( n = 3). C and D, Flow cytometry histograms and mean fluorescence intensity (MFI) of CRT on control or irradiated H460 ( C ) and PANC-1 ( D ) cells ( n = 3). Normalized to the control group. E, Immunofluorescence images of CRT (red) on control or irradiated H460 cells. F, Flow cytometry histograms and mean fluorescence intensity of tumor cells CRT from control or irradiated KPC tumor models ( n = 6). Normalized to the control group. G and H, Culture medium HMGB1 levels from control or irradiated H460 ( G ) and PANC-1 ( H ) cells measured by ELISA ( n = 3). I and J, Extracellular ATP release from control or irradiated H460 ( I ) and PANC-1 ( J ) cells measured by ELISA ( n = 3). K, scRNA-seq–derived M1 signature scores of tumor-associated macrophages from irradiated or control LLC tumors ( n = 3). L, Flow cytometry histograms and quantitation of control or irradiated H460 cell phagocytosis by THP-1 macrophages ( n = 3). M, Immunofluorescence images and quantitation of control or irradiated H460 cell (green) phagocytosis by THP-1 macrophages (red), with arrows indicating phagocytic events ( n = 6). Scale bars, 50 μm. N, Flow cytometry dotplot and quantitation of tumor cell phagocytosis by tumor-associated macrophages from control or irradiated LLC tumor ( n = 6). IR, 8 Gy irradiation. All data are presented as mean ± SEM and compared using a two-tailed Student t test. NS, not significant. A, Created in BioRender. Kong, L. (2026) https://BioRender.com/rwdzfwn .

Article Snippet: The human pancreatic ductal adenocarcinoma (PDAC) cell lines PANC-1 (RRID: CVCL_0480) and BxPC-3 (RRID: CVCL_0186), human non–small cell lung cancer cell lines NCI-H460 (RRID: CVCL_0459) and NCI-H1299 (RRID: CVCL_0060), human monocytic cell line THP-1 (RRID: CVCL_0006), murine hepatocellular carcinoma cell line Hepa1-6 (RRID: CVCL_0327), and murine lung carcinoma cell line Lewis (RRID: CVCL_4358) were obtained from the ATCC.

Techniques: Control, Irradiation, Flow Cytometry, Fluorescence, Immunofluorescence, Enzyme-linked Immunosorbent Assay, Derivative Assay, Quantitation Assay, Two Tailed Test

Radiation enhances tumor cell “do not eat me” signal CD24. A, UMAP plots of pancreatic adenocarcinoma with 10 clusters, NCBI Sequence Read Archive: GSE281288 . CD24 expression overlaid onto UMAP. B, Immunofluorescence images of CD24 (red) on control or irradiated H460 cells. Scale bars, 25 and 5 µm. C and D, Flow cytometry histograms and mean fluorescence intensity (MFI) of CD24 surface expression on control or irradiated H460 ( C ) and PANC-1 ( D ) cells ( n = 3). E, Tumor cell CD24 mean fluorescence intensity from control or irradiated KPC tumor models ( n = 6). F, Flow cytometry histograms and mean fluorescence intensity of CD24 surface expression on H460 cells 48 hours after 2–18 Gy of radiation ( n = 3). IR, 8 Gy irradiation. All data are presented as mean ± SEM and normalized to the control group. A two-tailed Student t test was performed for C–E . One-way ANOVA with a Tukey multiple comparisons test was performed for F . NS, not significant.

Journal: Cancer Research

Article Title: Radiation-Enhanced CD24 Membrane Trafficking via GPI Anchoring Mediates Antitumor Immune Evasion

doi: 10.1158/0008-5472.CAN-25-2616

Figure Lengend Snippet: Radiation enhances tumor cell “do not eat me” signal CD24. A, UMAP plots of pancreatic adenocarcinoma with 10 clusters, NCBI Sequence Read Archive: GSE281288 . CD24 expression overlaid onto UMAP. B, Immunofluorescence images of CD24 (red) on control or irradiated H460 cells. Scale bars, 25 and 5 µm. C and D, Flow cytometry histograms and mean fluorescence intensity (MFI) of CD24 surface expression on control or irradiated H460 ( C ) and PANC-1 ( D ) cells ( n = 3). E, Tumor cell CD24 mean fluorescence intensity from control or irradiated KPC tumor models ( n = 6). F, Flow cytometry histograms and mean fluorescence intensity of CD24 surface expression on H460 cells 48 hours after 2–18 Gy of radiation ( n = 3). IR, 8 Gy irradiation. All data are presented as mean ± SEM and normalized to the control group. A two-tailed Student t test was performed for C–E . One-way ANOVA with a Tukey multiple comparisons test was performed for F . NS, not significant.

Techniques: Sequencing, Expressing, Immunofluorescence, Control, Irradiation, Flow Cytometry, Fluorescence, Two Tailed Test

CD24 inhibition combined with radiation promotes macrophages phagocytosis and activation. A and B, Flow cytometry histograms of CD24 surface expression on H460 ( A ) and PANC-1 ( B ) cells transfected with CD24 -targeting siRNA (si CD24 ), negative-control siRNA (siNC), or isotype control. C and D, Flow cytometry histograms and quantitation of H460 ( C ) and PANC-1 ( D ) cell phagocytosis by THP-1 macrophages, with the indicated treatments ( n = 3). E, Immunofluorescence images and quantitation of H460 cell phagocytosis by THP-1 macrophages (red), with the indicated treatments (green). Arrows, phagocytic events ( n = 6). Scale bars, 50 μm. F, qRT-PCR analysis of Siglec- 10 in THP-1 macrophages transfected with si Siglec- 10 or siNC ( n = 3). G, Flow cytometry histograms and quantitation of irradiated H460 cell phagocytosis by THP-1 macrophages, with the indicated treatments ( n = 3). H – J, Flow cytometry histograms and mean fluorescence intensity (MFI) of CD80 ( H ), CD86 ( I ), and PD-L1 ( J ) on BMDMs cocultured with tumor cells, with the indicated treatments ( n = 3). IR, 8 Gy irradiation. All data are presented as mean ± SEM. One-way ANOVA with a Tukey multiple comparisons test was performed for C–E and G–J . A two-tailed Student t test was performed for F . NS, not significant.

Journal: Cancer Research

Article Title: Radiation-Enhanced CD24 Membrane Trafficking via GPI Anchoring Mediates Antitumor Immune Evasion

doi: 10.1158/0008-5472.CAN-25-2616

Figure Lengend Snippet: CD24 inhibition combined with radiation promotes macrophages phagocytosis and activation. A and B, Flow cytometry histograms of CD24 surface expression on H460 ( A ) and PANC-1 ( B ) cells transfected with CD24 -targeting siRNA (si CD24 ), negative-control siRNA (siNC), or isotype control. C and D, Flow cytometry histograms and quantitation of H460 ( C ) and PANC-1 ( D ) cell phagocytosis by THP-1 macrophages, with the indicated treatments ( n = 3). E, Immunofluorescence images and quantitation of H460 cell phagocytosis by THP-1 macrophages (red), with the indicated treatments (green). Arrows, phagocytic events ( n = 6). Scale bars, 50 μm. F, qRT-PCR analysis of Siglec- 10 in THP-1 macrophages transfected with si Siglec- 10 or siNC ( n = 3). G, Flow cytometry histograms and quantitation of irradiated H460 cell phagocytosis by THP-1 macrophages, with the indicated treatments ( n = 3). H – J, Flow cytometry histograms and mean fluorescence intensity (MFI) of CD80 ( H ), CD86 ( I ), and PD-L1 ( J ) on BMDMs cocultured with tumor cells, with the indicated treatments ( n = 3). IR, 8 Gy irradiation. All data are presented as mean ± SEM. One-way ANOVA with a Tukey multiple comparisons test was performed for C–E and G–J . A two-tailed Student t test was performed for F . NS, not significant.

Techniques: Inhibition, Activation Assay, Flow Cytometry, Expressing, Transfection, Negative Control, Control, Quantitation Assay, Immunofluorescence, Quantitative RT-PCR, Irradiation, Fluorescence, Two Tailed Test

Radiation enhances CD24 membrane trafficking via GPI anchoring. A and B, Western blot analysis of CD24 in control or irradiated H460 ( A ) and PANC-1 ( B ) whole-cell lysate. C, Schematic representation of GPI anchoring. D, Western blot analysis of CD24 in control or irradiated H460 cell membrane and cytosolic lysate. E, Proteomic analysis heatmap of differential proteins in control or irradiated H1299. F and G, Western blot analysis of GPAA1 in control or irradiated H460 ( F ) and PANC-1 ( G ) whole-cell lysate. H, Western blot analysis of GPAA1 and CD24 in H460 cells transfected with si GPAA1 or siNC. I, Flow cytometry histograms of CD24 surface expression on H460 cells, with the indicated treatment or isotype control ( n = 3). MFI, mean fluorescence intensity. J, Flow cytometry histograms and quantitation of H460 cell phagocytosis by THP-1 macrophages, with the indicated treatments ( n = 3). IR, 8 Gy irradiation. All data are presented as mean ± SEM and compared using one-way ANOVA with a Tukey multiple comparisons test. NS, not significant.

Journal: Cancer Research

Article Title: Radiation-Enhanced CD24 Membrane Trafficking via GPI Anchoring Mediates Antitumor Immune Evasion

doi: 10.1158/0008-5472.CAN-25-2616

Figure Lengend Snippet: Radiation enhances CD24 membrane trafficking via GPI anchoring. A and B, Western blot analysis of CD24 in control or irradiated H460 ( A ) and PANC-1 ( B ) whole-cell lysate. C, Schematic representation of GPI anchoring. D, Western blot analysis of CD24 in control or irradiated H460 cell membrane and cytosolic lysate. E, Proteomic analysis heatmap of differential proteins in control or irradiated H1299. F and G, Western blot analysis of GPAA1 in control or irradiated H460 ( F ) and PANC-1 ( G ) whole-cell lysate. H, Western blot analysis of GPAA1 and CD24 in H460 cells transfected with si GPAA1 or siNC. I, Flow cytometry histograms of CD24 surface expression on H460 cells, with the indicated treatment or isotype control ( n = 3). MFI, mean fluorescence intensity. J, Flow cytometry histograms and quantitation of H460 cell phagocytosis by THP-1 macrophages, with the indicated treatments ( n = 3). IR, 8 Gy irradiation. All data are presented as mean ± SEM and compared using one-way ANOVA with a Tukey multiple comparisons test. NS, not significant.

Techniques: Membrane, Western Blot, Control, Irradiation, Transfection, Flow Cytometry, Expressing, Fluorescence, Quantitation Assay

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