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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.
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
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Absolute Biotech Inc pancreatic duct epithelial cell line h6c7 hpde
Cancer-derived conditioned media induces apoptosis-related gene expression and dysfunction in NK cells Human primary NK cells were incubated with control media (RPMI), AsPC-1-CM, or Capan-2-CM, followed by functional and molecular analyses. (A) NK cells were treated with CM for 72 h and stained with Annexin V/7-aminoactinomycin D (7-AAD) to assess apoptosis. (B) Metabolic activity in NK cells after 24 h of CM exposure was measured by oxygen consumption rate (OCR) and extracellular acidification rate (ECAR). (C) CM-pretreated NK cells were co-cultured with AsPC-1-Luc or Capan-2-Luc cancer cells for 24 h, and cancer-cell-killing activity was measured. (D) Expression of apoptosis-related proteins BIM and NOXA in CM-treated NK cells was analyzed using western blotting. Representative blots show NOXA and BIM levels following 24 h exposure to CM derived from normal <t>pancreatic</t> epithelial cells <t>(HPDE)</t> or pancreatic cancer cell lines (AsPC-1 and Capan-2). BIM and NOXA protein levels were quantified from three independent experiments and normalized to β-actin. (E) Western blots showing the expression of NOXA and BIM in NK cells following 20 h exposure to IL-6, IL-10, or TGF-β1. All data are presented as mean ± standard error of the mean (SEM). p values were calculated using one-way ANOVA with multiple comparison tests (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001).
Pancreatic Duct Epithelial Cell Line H6c7 Hpde, supplied by Absolute Biotech Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Absolute Biotech Inc pancreatic duct epithelial hpde cell line h6c7
Cancer-derived conditioned media induces apoptosis-related gene expression and dysfunction in NK cells Human primary NK cells were incubated with control media (RPMI), AsPC-1-CM, or Capan-2-CM, followed by functional and molecular analyses. (A) NK cells were treated with CM for 72 h and stained with Annexin V/7-aminoactinomycin D (7-AAD) to assess apoptosis. (B) Metabolic activity in NK cells after 24 h of CM exposure was measured by oxygen consumption rate (OCR) and extracellular acidification rate (ECAR). (C) CM-pretreated NK cells were co-cultured with AsPC-1-Luc or Capan-2-Luc cancer cells for 24 h, and cancer-cell-killing activity was measured. (D) Expression of apoptosis-related proteins BIM and NOXA in CM-treated NK cells was analyzed using western blotting. Representative blots show NOXA and BIM levels following 24 h exposure to CM derived from normal <t>pancreatic</t> epithelial cells <t>(HPDE)</t> or pancreatic cancer cell lines (AsPC-1 and Capan-2). BIM and NOXA protein levels were quantified from three independent experiments and normalized to β-actin. (E) Western blots showing the expression of NOXA and BIM in NK cells following 20 h exposure to IL-6, IL-10, or TGF-β1. All data are presented as mean ± standard error of the mean (SEM). p values were calculated using one-way ANOVA with multiple comparison tests (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001).
Pancreatic Duct Epithelial Hpde Cell Line H6c7, supplied by Absolute Biotech Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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pancreatic duct epithelial hpde cell line h6c7 - by Bioz Stars, 2026-09
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ATCC hpde human normal ductal epithelial cell lines
Cancer-derived conditioned media induces apoptosis-related gene expression and dysfunction in NK cells Human primary NK cells were incubated with control media (RPMI), AsPC-1-CM, or Capan-2-CM, followed by functional and molecular analyses. (A) NK cells were treated with CM for 72 h and stained with Annexin V/7-aminoactinomycin D (7-AAD) to assess apoptosis. (B) Metabolic activity in NK cells after 24 h of CM exposure was measured by oxygen consumption rate (OCR) and extracellular acidification rate (ECAR). (C) CM-pretreated NK cells were co-cultured with AsPC-1-Luc or Capan-2-Luc cancer cells for 24 h, and cancer-cell-killing activity was measured. (D) Expression of apoptosis-related proteins BIM and NOXA in CM-treated NK cells was analyzed using western blotting. Representative blots show NOXA and BIM levels following 24 h exposure to CM derived from normal <t>pancreatic</t> epithelial cells <t>(HPDE)</t> or pancreatic cancer cell lines (AsPC-1 and Capan-2). BIM and NOXA protein levels were quantified from three independent experiments and normalized to β-actin. (E) Western blots showing the expression of NOXA and BIM in NK cells following 20 h exposure to IL-6, IL-10, or TGF-β1. All data are presented as mean ± standard error of the mean (SEM). p values were calculated using one-way ANOVA with multiple comparison tests (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001).
Hpde Human Normal Ductal Epithelial Cell Lines, 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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Absolute Biotech Inc human pancreatic duct epithelial hpde cell line h6c7
Cancer-derived conditioned media induces apoptosis-related gene expression and dysfunction in NK cells Human primary NK cells were incubated with control media (RPMI), AsPC-1-CM, or Capan-2-CM, followed by functional and molecular analyses. (A) NK cells were treated with CM for 72 h and stained with Annexin V/7-aminoactinomycin D (7-AAD) to assess apoptosis. (B) Metabolic activity in NK cells after 24 h of CM exposure was measured by oxygen consumption rate (OCR) and extracellular acidification rate (ECAR). (C) CM-pretreated NK cells were co-cultured with AsPC-1-Luc or Capan-2-Luc cancer cells for 24 h, and cancer-cell-killing activity was measured. (D) Expression of apoptosis-related proteins BIM and NOXA in CM-treated NK cells was analyzed using western blotting. Representative blots show NOXA and BIM levels following 24 h exposure to CM derived from normal <t>pancreatic</t> epithelial cells <t>(HPDE)</t> or pancreatic cancer cell lines (AsPC-1 and Capan-2). BIM and NOXA protein levels were quantified from three independent experiments and normalized to β-actin. (E) Western blots showing the expression of NOXA and BIM in NK cells following 20 h exposure to IL-6, IL-10, or TGF-β1. All data are presented as mean ± standard error of the mean (SEM). p values were calculated using one-way ANOVA with multiple comparison tests (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001).
Human Pancreatic Duct Epithelial Hpde Cell Line H6c7, supplied by Absolute Biotech Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Cell Biologics Inc hpde cells
Cancer-derived conditioned media induces apoptosis-related gene expression and dysfunction in NK cells Human primary NK cells were incubated with control media (RPMI), AsPC-1-CM, or Capan-2-CM, followed by functional and molecular analyses. (A) NK cells were treated with CM for 72 h and stained with Annexin V/7-aminoactinomycin D (7-AAD) to assess apoptosis. (B) Metabolic activity in NK cells after 24 h of CM exposure was measured by oxygen consumption rate (OCR) and extracellular acidification rate (ECAR). (C) CM-pretreated NK cells were co-cultured with AsPC-1-Luc or Capan-2-Luc cancer cells for 24 h, and cancer-cell-killing activity was measured. (D) Expression of apoptosis-related proteins BIM and NOXA in CM-treated NK cells was analyzed using western blotting. Representative blots show NOXA and BIM levels following 24 h exposure to CM derived from normal <t>pancreatic</t> epithelial cells <t>(HPDE)</t> or pancreatic cancer cell lines (AsPC-1 and Capan-2). BIM and NOXA protein levels were quantified from three independent experiments and normalized to β-actin. (E) Western blots showing the expression of NOXA and BIM in NK cells following 20 h exposure to IL-6, IL-10, or TGF-β1. All data are presented as mean ± standard error of the mean (SEM). p values were calculated using one-way ANOVA with multiple comparison tests (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001).
Hpde Cells, supplied by Cell Biologics Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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DSMZ normal human pancreatic epithelial cells hpde
Cancer-derived conditioned media induces apoptosis-related gene expression and dysfunction in NK cells Human primary NK cells were incubated with control media (RPMI), AsPC-1-CM, or Capan-2-CM, followed by functional and molecular analyses. (A) NK cells were treated with CM for 72 h and stained with Annexin V/7-aminoactinomycin D (7-AAD) to assess apoptosis. (B) Metabolic activity in NK cells after 24 h of CM exposure was measured by oxygen consumption rate (OCR) and extracellular acidification rate (ECAR). (C) CM-pretreated NK cells were co-cultured with AsPC-1-Luc or Capan-2-Luc cancer cells for 24 h, and cancer-cell-killing activity was measured. (D) Expression of apoptosis-related proteins BIM and NOXA in CM-treated NK cells was analyzed using western blotting. Representative blots show NOXA and BIM levels following 24 h exposure to CM derived from normal <t>pancreatic</t> epithelial cells <t>(HPDE)</t> or pancreatic cancer cell lines (AsPC-1 and Capan-2). BIM and NOXA protein levels were quantified from three independent experiments and normalized to β-actin. (E) Western blots showing the expression of NOXA and BIM in NK cells following 20 h exposure to IL-6, IL-10, or TGF-β1. All data are presented as mean ± standard error of the mean (SEM). p values were calculated using one-way ANOVA with multiple comparison tests (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001).
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
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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) 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

Cancer-derived conditioned media induces apoptosis-related gene expression and dysfunction in NK cells Human primary NK cells were incubated with control media (RPMI), AsPC-1-CM, or Capan-2-CM, followed by functional and molecular analyses. (A) NK cells were treated with CM for 72 h and stained with Annexin V/7-aminoactinomycin D (7-AAD) to assess apoptosis. (B) Metabolic activity in NK cells after 24 h of CM exposure was measured by oxygen consumption rate (OCR) and extracellular acidification rate (ECAR). (C) CM-pretreated NK cells were co-cultured with AsPC-1-Luc or Capan-2-Luc cancer cells for 24 h, and cancer-cell-killing activity was measured. (D) Expression of apoptosis-related proteins BIM and NOXA in CM-treated NK cells was analyzed using western blotting. Representative blots show NOXA and BIM levels following 24 h exposure to CM derived from normal pancreatic epithelial cells (HPDE) or pancreatic cancer cell lines (AsPC-1 and Capan-2). BIM and NOXA protein levels were quantified from three independent experiments and normalized to β-actin. (E) Western blots showing the expression of NOXA and BIM in NK cells following 20 h exposure to IL-6, IL-10, or TGF-β1. All data are presented as mean ± standard error of the mean (SEM). p values were calculated using one-way ANOVA with multiple comparison tests (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001).

Journal: Molecular Therapy Oncology

Article Title: Enhancing cancer killing and natural killer cell persistence by targeting NOXA, a predictor of poor patient survival

doi: 10.1016/j.omton.2026.201152

Figure Lengend Snippet: Cancer-derived conditioned media induces apoptosis-related gene expression and dysfunction in NK cells Human primary NK cells were incubated with control media (RPMI), AsPC-1-CM, or Capan-2-CM, followed by functional and molecular analyses. (A) NK cells were treated with CM for 72 h and stained with Annexin V/7-aminoactinomycin D (7-AAD) to assess apoptosis. (B) Metabolic activity in NK cells after 24 h of CM exposure was measured by oxygen consumption rate (OCR) and extracellular acidification rate (ECAR). (C) CM-pretreated NK cells were co-cultured with AsPC-1-Luc or Capan-2-Luc cancer cells for 24 h, and cancer-cell-killing activity was measured. (D) Expression of apoptosis-related proteins BIM and NOXA in CM-treated NK cells was analyzed using western blotting. Representative blots show NOXA and BIM levels following 24 h exposure to CM derived from normal pancreatic epithelial cells (HPDE) or pancreatic cancer cell lines (AsPC-1 and Capan-2). BIM and NOXA protein levels were quantified from three independent experiments and normalized to β-actin. (E) Western blots showing the expression of NOXA and BIM in NK cells following 20 h exposure to IL-6, IL-10, or TGF-β1. All data are presented as mean ± standard error of the mean (SEM). p values were calculated using one-way ANOVA with multiple comparison tests (∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001).

Article Snippet: The human pancreatic duct epithelial cell line (H6c7) (HPDE) was purchased from Kerafast (Boston, MA, USA) and cultured using Keratinocyte SFM (1X) kit (#17005042; Thermo Fisher Scientific, Waltham, MA, USA) with 1% AA solution according to the manufacturer’s growth conditions and subculturing method.

Techniques: Derivative Assay, Gene Expression, Incubation, Control, Functional Assay, Staining, Activity Assay, Cell Culture, Expressing, Western Blot, Comparison