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extra cellular matrix  (Celprogen Inc)


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    Celprogen Inc extra cellular matrix
    Extra Cellular Matrix, supplied by Celprogen Inc, used in various techniques. Bioz Stars score: 93/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/primary+pancreatic+cells/Human+Pancreatic+Normal+Primary+Cell+Culture+Extra-cellular+Matrix/pmc12448108-42-10-12
    Average 93 stars, based on 3 article reviews
    extra cellular matrix - by Bioz Stars, 2026-09
    93/100 stars

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    Cell Culture:

    Article Title: Insulin production from hiPSC-derived pancreatic cells in a novel wicking matrix bioreactor.
    Article Snippet: .. Primary pancreatic cells were purchased from Celprogen (Cat# 35002-04, Torrance, CA) and cultured on pre-coated flasks (Celprogen, Cat# E35002-04) according to manufacturer’s protocol. ..



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    The expression of EN2 in <t>HPNE,</t> <t>pancreatic</t> 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.
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    The expression of EN2 in <t>HPNE,</t> <t>pancreatic</t> 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.
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    ATCC human pancreatic ductal epithelial cells hpde
    Effect of tormentic acid on the proliferation of PDAC cells. (A) Chemical structure of tormentic acid. Viability of (B) PANC-1, (C) MIA PaCa-2 and (D) <t>HPDE</t> cells treated with various concentrations of tormentic acid, measured by the CCK-8 assay. (E) Phase contrast images of PANC-1 cells showed morphological changes following treatment with tormentic acid. Experiments were performed in triplicate, and data are presented as mean ± standard deviation. Images captured at ×20 magnification. *, P<0.05. CCK-8, Cell Counting Kit-8; PDAC, <t>pancreatic</t> ductal adenocarcinoma.
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    Effect of tormentic acid on the proliferation of PDAC cells. (A) Chemical structure of tormentic acid. Viability of (B) PANC-1, (C) MIA PaCa-2 and (D) <t>HPDE</t> cells treated with various concentrations of tormentic acid, measured by the CCK-8 assay. (E) Phase contrast images of PANC-1 cells showed morphological changes following treatment with tormentic acid. Experiments were performed in triplicate, and data are presented as mean ± standard deviation. Images captured at ×20 magnification. *, P<0.05. CCK-8, Cell Counting Kit-8; PDAC, <t>pancreatic</t> ductal adenocarcinoma.
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    Effect of tormentic acid on the proliferation of PDAC cells. (A) Chemical structure of tormentic acid. Viability of (B) PANC-1, (C) MIA PaCa-2 and (D) <t>HPDE</t> cells treated with various concentrations of tormentic acid, measured by the CCK-8 assay. (E) Phase contrast images of PANC-1 cells showed morphological changes following treatment with tormentic acid. Experiments were performed in triplicate, and data are presented as mean ± standard deviation. Images captured at ×20 magnification. *, P<0.05. CCK-8, Cell Counting Kit-8; PDAC, <t>pancreatic</t> ductal adenocarcinoma.
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    ATCC human pancreatic duct epithelial cells
    Collagen XVII expression is upregulated in PDAC cells upon interaction with CAFs. A, Western blot analysis of collagen XVII expression in immortalized human <t>pancreatic</t> ductal cells [human pancreatic duct <t>epithelial</t> (HPDE)], six PDAC cell lines, and telomerase reverse transcriptase–immortalized CAFs (CAF-1). β-Actin is shown as a loading control. B, COL17A1 expression in cell lines and matching xenograft tumors. C, Representative IHC staining of collagen XVII in cell line xenografts and PDXs of MGH1319. Scale bars, 50 μm. D, Schematic of the experimental setup of coculture and FACS of PDAC and CAF-1 cells. E, Collagen XVII expression in MGH1319 cells in monoculture and after coculture with CAF-1. β-Actin is shown as a loading control. F–H, Relative COL17A1 expression in MGH1319, MGH1275, MGH1108, and CAF-1 after mono- and coculture. The average (±SEM) from three independent experiments is shown. *, P < 0.05; ****, P < 0.0001; ns, not signficant (unpaired t test).
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    Image Search Results


    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.

    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

    Overexpression of EN2 in HPNE cells induces cellular transformation and stemness. (A and B) HPNE cells were stably transduced with lentiviral particles expressing either empty vector or EN2 cDNA. EN2 expression was measured by immunocytochemistry and qRT‐PCR. Blue colour = nuclei; Green colour = EN2. Data represent mean ( n = 4) ± SD. * = significantly different from HPNE/Empty Vector group ( p < 0.05). (C), Spheroid formation in suspension. Spheroid formation of HPNE/Empty Vector and HPNE/EN2 cDNA cells was measured. Spheroids in suspensions were photographed (left) and counted (right). Data represent mean ( n = 4) ± SD. # = significantly different between groups ( p < 0.05). (D), Expression of stem cell markers. RNA was isolated, and expression of stem cell markers (CD24, CD44, CD133 and LGR5) was measured by qRT‐PCR. GAPDH was used as an internal control. Data represent mean ( n = 4) ± SD. * = significantly different from HPNE/Empty Vector group ( p < 0.05). Gene expression of Empty Vector was normalised to 1. (E), Expression of pluripotency‐maintaining factors. RNA was isolated, and the expression of pluripotency‐maintaining factors (Oct4, Sox2, cMyc and KLF4) was measured by qRT‐PCR analysis. GAPDH was used as an internal control. Data represent mean ( n = 4) ± SD. * = significantly different from HPNE/Empty Vector group ( p < 0.05). Gene expression of Empty Vector was normalised to 1.

    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: Overexpression of EN2 in HPNE cells induces cellular transformation and stemness. (A and B) HPNE cells were stably transduced with lentiviral particles expressing either empty vector or EN2 cDNA. EN2 expression was measured by immunocytochemistry and qRT‐PCR. Blue colour = nuclei; Green colour = EN2. Data represent mean ( n = 4) ± SD. * = significantly different from HPNE/Empty Vector group ( p < 0.05). (C), Spheroid formation in suspension. Spheroid formation of HPNE/Empty Vector and HPNE/EN2 cDNA cells was measured. Spheroids in suspensions were photographed (left) and counted (right). Data represent mean ( n = 4) ± SD. # = significantly different between groups ( p < 0.05). (D), Expression of stem cell markers. RNA was isolated, and expression of stem cell markers (CD24, CD44, CD133 and LGR5) was measured by qRT‐PCR. GAPDH was used as an internal control. Data represent mean ( n = 4) ± SD. * = significantly different from HPNE/Empty Vector group ( p < 0.05). Gene expression of Empty Vector was normalised to 1. (E), Expression of pluripotency‐maintaining factors. RNA was isolated, and the expression of pluripotency‐maintaining factors (Oct4, Sox2, cMyc and KLF4) was measured by qRT‐PCR analysis. GAPDH was used as an internal control. Data represent mean ( n = 4) ± SD. * = significantly different from HPNE/Empty Vector group ( p < 0.05). Gene expression of Empty Vector was normalised to 1.

    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: Over Expression, Transformation Assay, Stable Transfection, Transduction, Expressing, Plasmid Preparation, Immunocytochemistry, Quantitative RT-PCR, Suspension, Isolation, Control, Gene Expression

    Overexpression of EN2 in HPNE cells enhances cell motility and modulates expression of EMT‐related genes. (A) Cell Motility. HPNE cells were stably transduced with lentiviral particles expressing either empty vector or EN2 cDNA. (B) Expression of EMT‐related genes. RNA was isolated, and the EMT‐related genes (E‐cadherin, N‐cadherin, Snail, Slug, and Zeb1) were measured by qRT‐PCR analysis. GAPDH was used as an internal control. Data represent mean ( n = 4) ± SD. * = significantly different from HPNE/Empty Vector group ( p < 0.05). Gene expression of Empty Vector was normalised to 1.

    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: Overexpression of EN2 in HPNE cells enhances cell motility and modulates expression of EMT‐related genes. (A) Cell Motility. HPNE cells were stably transduced with lentiviral particles expressing either empty vector or EN2 cDNA. (B) Expression of EMT‐related genes. RNA was isolated, and the EMT‐related genes (E‐cadherin, N‐cadherin, Snail, Slug, and Zeb1) were measured by qRT‐PCR analysis. GAPDH was used as an internal control. Data represent mean ( n = 4) ± SD. * = significantly different from HPNE/Empty Vector group ( p < 0.05). Gene expression of Empty Vector was normalised to 1.

    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: Over Expression, Expressing, Stable Transfection, Transduction, Plasmid Preparation, Isolation, Quantitative RT-PCR, Control, Gene Expression

    The expression of miR-641 in pancreatic cancer. A The expression of miR-641 in 60 paired pancreatic cancer tumor tissue and non-tumor tissue was explored by qPCR. B The expression of miR-641 in different stages of pancreatic carcinoma patients. * P < 0.05, ** P < 0.01. C Kaplan–Meier analysis showed that higher expression of miR-641 predicted poor survival rate of pancreatic cancer patients. D The expression of miR-641 in pancreatic cancer cells (SW1990, CFPAC-1, BxPC-3 and PANC-1) and normal human pancreatic ductal epithelial cells (HPDE6-C7) was examined by qRT-PCR. ** P < 0.01 vs. HPDE6-C7. Data was shown as mean ± SD

    Journal: Discover Oncology

    Article Title: MiR-641 targets TMEFF2/MEK/PI3K to promote stem cell characteristics of pancreatic cancer cells

    doi: 10.1007/s12672-026-04584-2

    Figure Lengend Snippet: The expression of miR-641 in pancreatic cancer. A The expression of miR-641 in 60 paired pancreatic cancer tumor tissue and non-tumor tissue was explored by qPCR. B The expression of miR-641 in different stages of pancreatic carcinoma patients. * P < 0.05, ** P < 0.01. C Kaplan–Meier analysis showed that higher expression of miR-641 predicted poor survival rate of pancreatic cancer patients. D The expression of miR-641 in pancreatic cancer cells (SW1990, CFPAC-1, BxPC-3 and PANC-1) and normal human pancreatic ductal epithelial cells (HPDE6-C7) was examined by qRT-PCR. ** P < 0.01 vs. HPDE6-C7. Data was shown as mean ± SD

    Article Snippet: In the present work, we obtained pancreatic cancer cells (SW1990, CFPAC-1, BxPC-3 and PANC-1) and normal human pancreatic ductal epithelial cells (HPDE6-C7) in American Type Culture Collection (ATCC, Manassas, VA, USA) and fostered them individually within Dulbecco’s modified Eagle’s medium (DMEM, Zeye Biotechnology, Shanghai, China) that contained 10% fetal bovine serum (FBS, Beyotime, Shanghai, China) under 37 °C with 5% CO 2 .

    Techniques: Expressing, Quantitative RT-PCR

    Effect of tormentic acid on the proliferation of PDAC cells. (A) Chemical structure of tormentic acid. Viability of (B) PANC-1, (C) MIA PaCa-2 and (D) HPDE cells treated with various concentrations of tormentic acid, measured by the CCK-8 assay. (E) Phase contrast images of PANC-1 cells showed morphological changes following treatment with tormentic acid. Experiments were performed in triplicate, and data are presented as mean ± standard deviation. Images captured at ×20 magnification. *, P<0.05. CCK-8, Cell Counting Kit-8; PDAC, pancreatic ductal adenocarcinoma.

    Journal: Translational Cancer Research

    Article Title: A pentacyclic triterpene tormentic acid inhibits the proliferation and migration of pancreatic ductal adenocarcinoma cells

    doi: 10.21037/tcr-2025-1050

    Figure Lengend Snippet: Effect of tormentic acid on the proliferation of PDAC cells. (A) Chemical structure of tormentic acid. Viability of (B) PANC-1, (C) MIA PaCa-2 and (D) HPDE cells treated with various concentrations of tormentic acid, measured by the CCK-8 assay. (E) Phase contrast images of PANC-1 cells showed morphological changes following treatment with tormentic acid. Experiments were performed in triplicate, and data are presented as mean ± standard deviation. Images captured at ×20 magnification. *, P<0.05. CCK-8, Cell Counting Kit-8; PDAC, pancreatic ductal adenocarcinoma.

    Article Snippet: Human PDAC cell lines PANC-1 (ATCC ® CRL-1469TM, RRID:CVCL_0480) and MIA PaCa-2 (ATCC ® CRM-CRL-1420TM, RRID:CVCL_0428), along with normal human pancreatic ductal epithelial cells HPDE (HPDE6-C7, RRID:CVCL_4376), were obtained from the American Type Culture Collection (ATCC) and relevant sources.

    Techniques: CCK-8 Assay, Standard Deviation, Cell Counting

    Collagen XVII expression is upregulated in PDAC cells upon interaction with CAFs. A, Western blot analysis of collagen XVII expression in immortalized human pancreatic ductal cells [human pancreatic duct epithelial (HPDE)], six PDAC cell lines, and telomerase reverse transcriptase–immortalized CAFs (CAF-1). β-Actin is shown as a loading control. B, COL17A1 expression in cell lines and matching xenograft tumors. C, Representative IHC staining of collagen XVII in cell line xenografts and PDXs of MGH1319. Scale bars, 50 μm. D, Schematic of the experimental setup of coculture and FACS of PDAC and CAF-1 cells. E, Collagen XVII expression in MGH1319 cells in monoculture and after coculture with CAF-1. β-Actin is shown as a loading control. F–H, Relative COL17A1 expression in MGH1319, MGH1275, MGH1108, and CAF-1 after mono- and coculture. The average (±SEM) from three independent experiments is shown. *, P < 0.05; ****, P < 0.0001; ns, not signficant (unpaired t test).

    Journal: Cancer Research Communications

    Article Title: Collagen XVII Promotes Pancreatic Ductal Adenocarcinoma Tumor Growth through Regulation of PIK3R5

    doi: 10.1158/2767-9764.CRC-24-0392

    Figure Lengend Snippet: Collagen XVII expression is upregulated in PDAC cells upon interaction with CAFs. A, Western blot analysis of collagen XVII expression in immortalized human pancreatic ductal cells [human pancreatic duct epithelial (HPDE)], six PDAC cell lines, and telomerase reverse transcriptase–immortalized CAFs (CAF-1). β-Actin is shown as a loading control. B, COL17A1 expression in cell lines and matching xenograft tumors. C, Representative IHC staining of collagen XVII in cell line xenografts and PDXs of MGH1319. Scale bars, 50 μm. D, Schematic of the experimental setup of coculture and FACS of PDAC and CAF-1 cells. E, Collagen XVII expression in MGH1319 cells in monoculture and after coculture with CAF-1. β-Actin is shown as a loading control. F–H, Relative COL17A1 expression in MGH1319, MGH1275, MGH1108, and CAF-1 after mono- and coculture. The average (±SEM) from three independent experiments is shown. *, P < 0.05; ****, P < 0.0001; ns, not signficant (unpaired t test).

    Article Snippet: Immortalized epithelial cells from normal human pancreatic duct epithelial cells were purchased from ATCC.

    Techniques: Expressing, Western Blot, Reverse Transcription, Control, Immunohistochemistry