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97
ATCC human normal pancreatic ductal epithelial cells hpne
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.
Human Normal Pancreatic Ductal Epithelial Cells Hpne, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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96
ATCC human pancreatic normal ductal epithelial cell line htert hpne
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.
Human Pancreatic Normal Ductal Epithelial Cell Line Htert Hpne, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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97
ATCC normal human pancreatic ductal epithelial cells
The expression of miR-641 in <t>pancreatic</t> 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 <t>epithelial</t> cells <t>(HPDE6-C7)</t> was examined by qRT-PCR. ** P < 0.01 vs. HPDE6-C7. Data was shown as mean ± SD
Normal Human Pancreatic Ductal Epithelial Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/normal human pancreatic ductal epithelial cells/product/ATCC
Average 97 stars, based on 1 article reviews
normal human pancreatic ductal epithelial cells - by Bioz Stars, 2026-05
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99
ATCC human pancreatic duct epithelial cell line
The expression of miR-641 in <t>pancreatic</t> 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 <t>epithelial</t> cells <t>(HPDE6-C7)</t> was examined by qRT-PCR. ** P < 0.01 vs. HPDE6-C7. Data was shown as mean ± SD
Human Pancreatic Duct Epithelial Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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97
ATCC human pancreatic duct normal epithelial cells hpne
The expression of miR-641 in <t>pancreatic</t> 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 <t>epithelial</t> cells <t>(HPDE6-C7)</t> was examined by qRT-PCR. ** P < 0.01 vs. HPDE6-C7. Data was shown as mean ± SD
Human Pancreatic Duct Normal Epithelial Cells Hpne, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/human pancreatic duct normal epithelial cells hpne/product/ATCC
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97
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.
Human Pancreatic Ductal Epithelial Cells Hpde, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/human pancreatic ductal epithelial cells hpde/product/ATCC
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human pancreatic ductal epithelial cells hpde - by Bioz Stars, 2026-05
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97
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).
Human Pancreatic Duct Epithelial Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/human pancreatic duct epithelial cells/product/ATCC
Average 97 stars, based on 1 article reviews
human pancreatic duct epithelial cells - by Bioz Stars, 2026-05
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90
DSMZ normal human pancreatic epithelial cells hpde
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).
Normal Human Pancreatic Epithelial Cells Hpde, supplied by DSMZ, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/normal human pancreatic epithelial cells hpde/product/DSMZ
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normal human pancreatic epithelial cells hpde - by Bioz Stars, 2026-05
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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