Increase in calcitonin mRNA levels in rats at high risk of C cell tumours is genetically determined

• Published in: Biochemical and biophysical research communications Vol. 167; no. 1; pp. 232 - 237
• Main Authors: Delehaye, M.C., Bouizar, Z., Minvielle, S., Pidoux, E., Segond, N., Treilhou-Lahille, F., Milhaud, G., Moukhtar, M.S.
• Format: Journal Article
• Language: English
• Published: San Diego, CA Elsevier Inc 28.02.1990; Elsevier
• Subjects: Aminoacids, peptides. Hormones. Neuropeptides; Analytical, structural and metabolic biochemistry; Animals; Autoradiography; Biological and medical sciences; Blotting, Northern; Calcitonin - genetics; Calcitonin - metabolism; Carcinoma - genetics; Carcinoma - metabolism; Disease Susceptibility; Female; Fundamental and applied biological sciences. Psychology; Male; Nucleic Acid Hybridization; Proteins; Radioimmunoassay; Rats; Risk Factors; RNA, Messenger - analysis; Thyroid Neoplasms - genetics; Thyroid Neoplasms - metabolism; Vertebrata; Mammalia; Messenger RNA; Rat; Calcitonin; Rodentia; Peptide hormone; Thyroid hormone; Tumor; Gene expression; Neuropeptide; Quantitative analysis
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/0006-291X(90)91755-H

C-cells tumours are frequent (50%) in old WAG Rij rats. In comparison to the original Wistar strain, three month old WAG Rij rats are characterized by higher calcitonin synthesis and secretion, in addition to a genetically transmitted loss of calcitonin binding sites in the outer renal medulla. In order to determine if the increase of calcitonin gene expression is also of genetic origin, we quantified calcitonin and its specific messenger in the thyroid glands of second generation (Wistar × WAG Rij ) hybrids. These parameters ranged from low Wistar like to higher WAG Rij like values. The amount of calcitonin messenger in the thyroid was highly correlated to the release of the hormone in plasma elicited by a calcium challenge and inversely correlated with the number of its binding sites in the kidney. Our results suggest that an enhanced expression of the calcitonin gene is genetically transmitted, probably as a consequence of the mutation involved in the loss of renal calcitonin binding sites. It may represent the first event leading to malignancy.