title: Differences in molecular biological, biological and growth characteristics between the immortal and malignant hamster pancreatic cells.
abstract: We compared morphological, biological and molecular biological patterns of a newly established, spontaneously immortalized pancreatic ductal cell line, TAKA-1, with a hamster pancreatic ductal adenocarcinoma cell line, PC-1. PC-1 cells grew in a monolayer on plastic tissue culture flasks, whereas TAKA-1 cells required type I collagen gel matrix to propagate. The growth rate and argyrophilic nuclear organizer region (Ag-NOR) counts were greater in PC-1 cells than in TAKA-1 cells. More TAKA-1 cells were in G0/G1 and less were in the S cell cycle phase than PC-1 cells. Karyotypically, the consistent change in TAKA-1 cells was an abnormal no. 3 chromosome, whereas additional chromosomal abnormalities were found in PC-1 cells. Ultrastructurally, TAKA-1 cells formed ductal structures and were composed of two types of cells, as in the normal hamster pancreatic ducts, whereas PC-1 cells were pleomorphic, showed evidence for loss of differentiation and contained intracytoplasmic lumens. Unlike the PC-1, TAKA-1 cells did not show a point mutation at codon 12 in the c-Ki-ras oncogene and did not grow in soft agar. Receptor binding assay showed specific epidermal growth factor binding to both cell lines, but secretin binding only to TAKA-1 cells. Both cells produced and released transforming growth factor-alpha in serum-free medium. Both cell lines expressed blood group A antigen, carbonic anhydrase, coexpressed cytokeratin and vimentin, and reacted with tomato and Phaseolus vulgaris leucoagglutinin (L-PHA) lectins. The results demonstrate that chromosomal abnormalities, cell cycle patterns, expression of cytokeratin 18, lectin bindings and the c-Ki-ras mutation are the features that distinguish the benign from the malignant pancreatic ductal cells in Syrian hamster.
authors.affiliation: Eppley Institute for Research in Cancer, University of Nebraska Medical Center, Omaha, USA.
authors.forename: T
authors.initials: T
authors.lastname: Takahashi
authors.forename: M P
authors.initials: MP
authors.lastname: Moyer
authors.forename: M
authors.initials: M
authors.lastname: Cano
authors.forename: Q J
authors.initials: QJ
authors.lastname: Wang
authors.forename: C P
authors.initials: CP
authors.lastname: Mountjoy
authors.forename: W
authors.initials: W
authors.lastname: Sanger
authors.forename: T E
authors.initials: TE
authors.lastname: Adrian
authors.forename: H
authors.initials: H
authors.lastname: Sugiura
authors.forename: H
authors.initials: H
authors.lastname: Katoh
authors.forename: P M
authors.initials: PM
authors.lastname: Pour
mesh_terms: D000230:Adenocarcinoma / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D000818:Animals; D001483:Base Sequence; D002448:Cell Adhesion / Q000502:physiology; D002453:Cell Cycle / Q000502:physiology; D002455:Cell Division / Q000187:drug effects / Q000502:physiology; D002460:Cell Line; D002766:Cholecystokinin / Q000378:metabolism; D006224:Cricetinae; D004815:Epidermal Growth Factor / Q000494:pharmacology; D005434:Flow Cytometry; D019886:Gastrin-Releasing Peptide; D011905:Genes, ras; D007150:Immunohistochemistry; D007621:Karyotyping; D007700:Kinetics; D008027:Light; D008647:Mesocricetus; D008853:Microscopy; D008854:Microscopy, Electron; D008969:Molecular Sequence Data; D010179:Pancreas / Q000166:cytology* / Q000187:drug effects / Q000502:physiology; D010183:Pancreatic Ducts / Q000166:cytology* / Q000473:pathology; D010190:Pancreatic Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D010455:Peptides / Q000378:metabolism; D017354:Point Mutation; D012633:Secretin / Q000378:metabolism; D014407:Tumor Cells, Cultured / Q000187:drug effects
chemical_list: D010455:Peptides; D012633:Secretin; D004815:Epidermal Growth Factor; D019886:Gastrin-Releasing Peptide; D002766:Cholecystokinin