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Publication Detail
Calcitonin receptor mRNA expression in TT cells: effect of dexamethasone.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Frendo JL, Delage-Mourroux R, Cohen R, Pichaud F, Pidoux E, Guliana JM, Jullienne A
  • Publication date:
  • Pagination:
    37, 43
  • Journal:
    Mol Cell Endocrinol
  • Volume:
  • Issue:
  • Status:
  • Country:
  • Print ISSN:
  • PII:
  • Language:
  • Keywords:
    Autocrine Communication, Calcitonin, Carcinoma, Medullary, Cell Division, Dexamethasone, Gene Expression Regulation, Neoplastic, Glucocorticoids, Humans, RNA, Messenger, RNA, Neoplasm, Receptors, Calcitonin, Thyroid Neoplasms, Tumor Cells, Cultured
Among the four isoforms of the calcitonin receptor (CTR) described in humans, two differ by the presence of h-CTR1 or absence of h-CTR2 of 16 amino acids in the first intracellular loop. Both receptors are biologically active. The TT cell line derived from a human medullary carcinoma of the thyroid is characterized by the secretion of large amounts of calcitonin. We have recently shown that this cell line expresses h-CTR2. In the present work we have studied the expression of CTR during TT cell proliferation and used dexamethasone to modify calcitonin expression in order to establish if an autocrine regulation involving calcitonin and its receptor was functional in the TT cells. The expression of this receptor and of calcitonin during TT cell proliferation was studied by reverse transcriptase-polymerase chain reaction (RT-PCR). Dexamethasone, a potent inhibitor of TT cell proliferation, levels (day 6 of culture) specifically increased receptor levels from day 8 onwards. CT peptide and CT mRNA levels decreased or were similar during experimental time. CTR regulation by glucocorticoids is suggested in TT cells. Autocrine regulation of CTR is also suggested by relation between CT mRNA levels and CTR mRNA.
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