Immortalized Human Pancreatic Duct Epithelial Cells (HPDE6c7)

Cat.No.: CSC-I2298Z

Species: homo sapiens

Morphology: Polygonal

Culture Properties: Adherent

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Cat.No.
CSC-I2298Z
Description
Immortalized Human Pancreatic Duct Epithelial Cells (HPDE6c7) demonstrates a near normal genotype and phenotype of pancreatic duct epithelial cells. Immortalized Human Pancreatic Duct Epithelial Cells (HPDE6c7) retain normal Ki-ras, p53, C-myc, and p16INK4A genotypes but lack the p53 functional pathway.Immortalized Human Pancreatic Duct Epithelial Cells (HPDE6c7) are useful for studies on the molecular basis of pancreatic duct cell carcinogenesis and islet cell differentiation. Immortalized Human Pancreatic Duct Epithelial Cells (HPDE6c7) are a versatile model for the pancreatic ductal epithelium, facilitating the development of strategies for the chemoprevention of human pancreatic cancers. Immortalized Human Pancreatic Duct Epithelial Cells (HPDE6c7) originated from normal human pancreatic duct of a 63-year-old female, having been genotypically altered by infection with retrovirus vector expressing E6E7 genes of human papilloma virus (HPV)-16.3
Species
homo sapiens
Recommended Medium
SuperCult® Immortalized Human Pancreatic Duct Epithelial Cell Medium (Cat No.: CM-I2298Z)
Freezing Medium
Complete medium supplemented with 10% (v/v) DMSO
Culture Properties
Adherent
Morphology
Polygonal
Application
For Research Use Only
Growth Properties
Cells are cultured as a monolayer at 37°C in a humidified atmosphere with 5% CO2.
Citation Guidance
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HPDE6c7, also designated HPDE6-E6E7c7 or H6c7, is an immortalized but non‑tumorigenic human pancreatic duct epithelial cell line established from the normal pancreatic duct of a 63‑year‑old female donor. Immortalization was achieved by transduction of a retrovirus vector carrying the E6 and E7 genes of human papillomavirus type 16 (HPV‑16) into primary normal human pancreatic duct epithelial (HPDE) cells. Single clones were isolated that retain a near‑normal genotype and phenotype of pancreatic duct epithelium.

The defining advantage of the HPDE6c7 line is its exceptionally close resemblance to normal pancreatic duct epithelium, combined with an indefinite proliferative lifespan. The cells exhibit anchorage‑dependent growth, are non‑tumorigenic in SCID mice, and express definitive ductal lineage markers including carbonic anhydrase II, MUC‑1, and cytokeratins 7, 8, 18 and 19. Importantly, HPDE6c7 cells retain normal genotypes of Ki‑ras, p53, C‑myc, and p16ᴵᴺᴷ⁴ᴬ, with the only identifiable aberration being the loss of functional p53 pathway due to E6‑mediated degradation. This near‑normal status distinguishes HPDE6c7 from pancreatic cancer cell lines, which harbor numerous driver mutations and exhibit aberrant phenotypes.

HPDE6c7 cells are a versatile and physiologically relevant model for the pancreatic ductal epithelium, widely applied in studies of pancreatic duct carcinogenesis, islet cell differentiation, and chemoprevention of pancreatic cancer. They also serve as a genetically stable baseline for stepwise introduction of PDAC‑associated alterations to model multistep pancreatic oncogenesis.

Mitochondrial Calcium Uniporter Promotes Mitophagy in Caerulein‑Treated Pancreatic Ductal Epithelial Cells

The mitochondrial calcium uniporter (MCU) is a major protein for the uptake of mitochondrial calcium to regulate intracellular energy metabolism, including processes such as mitophagy. The present study investigated the effect of the MCU on mitophagy in pancreatic ductal epithelial cells (PDECs) in acute pancreatitis (AP) in vitro. The normal human PDECs (HPDE6‑C7) were treated with caerulein (CAE) to induce AP‑like changes, with or without ruthenium red to inhibit the MCU. The mitochondrial membrane potentials (MMPs) and mitochondrial Ca2+ levels were analyzed by fluorescence. The expression levels of MCU, LC3, p62, and translocase of the outer mitochondrial membrane complex subunit 20 (TOMM20), putative kinase 1 (PINK1), and Parkin were measured by western blotting and immunofluorescence. Mitophagy was observed by confocal fluorescence microscopy and transmission electron microscopy.

The results showed that CAE increased the MCU protein expression, mitochondrial Ca2+ levels, MMP depolarization and the protein expression of mitophagy markers including the LC3II/I ratio, PINK1, and Parkin. CAE decreased the protein expression of p62 and TOMM20, and promoted the formation of mitophagosomes in HPDE6‑C7 cells. Notably, changes in these markers were reversed by inhibiting the MCU.

Inhibition of MCU attenuated CAE-induced mitophagy in HPDE6-C7 cells.

Fig. 1. Ruthenium red treatment inhibited CAE-induced mitophagy in HPDE6-C7 cells (Lei, Yu, et al., 2024).

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