human pdac cell lines panc 1 (ATCC)
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Human Pdac Cell Lines Panc 1, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 7924 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 99 stars, based on 7924 article reviews
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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
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
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
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
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
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
