Differences in molecular biological, biological and growth characteristics between the immortal and malignant hamster pancreatic cells

• Published in: Carcinogenesis (New York) 1995-04, Vol.16 (4), p.931-939
• Main Authors: Takahashi, Toshiyuki, Moyer, Mary P., Cano, Martin, Wang, Qiming J., Mountjoy, Charles P., Sanger, Warren, Adrian, Thomas E., Sugiura, Hiroshi, Katoh, Hiroyuki, Pour, Parviz M.
• Format: Article
• Language: English
• Subjects: Adenocarcinoma - genetics; Adenocarcinoma - metabolism; Adenocarcinoma - pathology; Animal tumors. Experimental tumors; Animals; Base Sequence; Biological and medical sciences; Cell Adhesion - physiology; Cell Cycle - physiology; Cell Division - drug effects; Cell Division - physiology; Cell Line; Cholecystokinin - metabolism; Cricetinae; Epidermal Growth Factor - pharmacology; Experimental digestive system and abdominal tumors; Flow Cytometry; Gastrin-Releasing Peptide; Genes, ras; Immunohistochemistry; Karyotyping; Kinetics; Light; Medical sciences; Mesocricetus; Microscopy; Microscopy, Electron; Molecular Sequence Data; Pancreas - cytology; Pancreas - drug effects; Pancreas - physiology; Pancreatic Ducts - cytology; Pancreatic Ducts - pathology; Pancreatic Neoplasms - genetics; Pancreatic Neoplasms - metabolism; Pancreatic Neoplasms - pathology; Peptides - metabolism; Point Mutation; Secretin - metabolism; Tumor Cells, Cultured - drug effects; Tumors
• ISSN: 0143-3334; 1460-2180
• DOI: 10.1093/carcin/16.4.931

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-α 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.