Characterization of a newly established human pancreatic carcinoma cell line, UK Pan-1

Cancer. 2000 May 1;88(9):2010-21. doi: 10.1002/(sici)1097-0142(20000501)88:9<2010::aid-cncr5>3.0.co;2-5.

Abstract

Background: A highly tumorigenic cell line designated as UK Pan-1 was established in a surgically removed human pancreatic adenocarcinoma and characterized as having many of the genotypic and phenotypic alterations commonly found in pancreatic tumors.

Methods: The cell line was characterized by its morphology, growth rate in monolayer culture and soft agar, tumorigenicity in nude mice, and chromosomal analysis. Furthermore, the status of p53, Ki-ras mutation and transforming growth factor (TGF)-/receptor expression were determined. The characteristics of UK Pan-1 were compared with those of other commonly used pancreatic carcinoma cell lines.

Results: Quiescent UK Pan-1 cells could be stimulated to proliferate in growth factor free nutrient media, indicating a growth factor independent phenotype. UK Pan- 1 cells grew in soft agar and rapidly formed tumors in nude mice. This cell line possesses a mutation at codon 12 of the c-Ki-ras-2 gene that is commonly found in pancreatic carcinoma. Fluorescence in situ hybridization showed that two alleles of p53 tumor suppressor gene were present in UK Pan-1. However, sequencing analysis revealed a mutation in one allele at exon 8, codon 273 (G to A; Arg to His). Additional growth assays indicated that the cell line was insensitive to negative growth regulation induced by exogenous TGF-beta. Molecular analysis of the TGF-beta signaling pathway showed that UK Pan-1 did not express appreciable levels of the TGF-beta receptor type I, II, or III mRNAs, but did express DPC4 mRNA. Karyotype analysis revealed an 18q21 deletion indicating a possible loss of heterozygosity for DPC4, as well as other chromosomal deletions and rearrangements.

Conclusions: This study indicates that UK Pan-1 is a highly tumorigenic cell line possessing a molecularly complex pattern of mutations that may be used as a model to further the understanding of the mechanisms responsible for the development of pancreatic carcinoma.

Publication types

  • Comparative Study
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adenocarcinoma / genetics
  • Adenocarcinoma / pathology*
  • Alleles
  • Animals
  • Cell Division
  • Codon / genetics
  • Culture Media
  • DNA-Binding Proteins / genetics
  • Exons / genetics
  • Gene Expression Regulation, Neoplastic
  • Genes, p53 / genetics
  • Genes, ras / genetics
  • Genotype
  • Humans
  • Loss of Heterozygosity / genetics
  • Male
  • Mice
  • Mice, Nude
  • Mutation / genetics
  • Neoplasm Transplantation
  • Pancreatic Neoplasms / genetics
  • Pancreatic Neoplasms / pathology*
  • Phenotype
  • Point Mutation / genetics
  • Receptors, Transforming Growth Factor beta / genetics
  • Signal Transduction / genetics
  • Smad4 Protein
  • Trans-Activators / genetics
  • Transforming Growth Factor beta / genetics
  • Tumor Cells, Cultured*

Substances

  • Codon
  • Culture Media
  • DNA-Binding Proteins
  • Receptors, Transforming Growth Factor beta
  • SMAD4 protein, human
  • Smad4 Protein
  • Smad4 protein, mouse
  • Trans-Activators
  • Transforming Growth Factor beta