Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:Q9NVM9 (GCT1)
 7 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have recently found the presence of many binuclear cells among isolated and smeared cells in giant cell tumor of the bone (GCT). These binuclear cells are possibly associated with the formation of multinuclear cells. Therefore, this study was undertaken to clarify the mechanism of binucleation in GCT, using primary culture cells exposed to acridine orange (AO) which is a fluorescent vital staining dye for the cytoplasm and nucleus and which inhibits mitosis. The cells were isolated from explants of fresh tumor materials obtained from two GCT patients (GCT1 and GCT2). These cells were cultured in Dulbecco's modified Eagle medium (DMEM) with 10% Fetal calf serum (FCS). After exposure to 0.5 microgram/ml AO, for 0, 6, 24, 48, 96 and 144 hours the following parameters were investigated: 1) cell growth rate (GR); 2) frequency of hyperdiploid cells (%HDC) by DNA cytofluorometry; 3) mitotic index (MI); 4) BrdU labeling index (LI); 5) frequency of binuclear cells (%BNC). Compared to the control cells which were cultured in AO-free medium, the GR of both GCT cells exposed to AO was remarkably inhibited. The MI was 0 from 24 to 144 hours. The %HDC was increased at 24 hours and was maintained high until 144 hours. The LI was temporarily increased at 6 hours, but was decreased at 48 hours. The %BNC was gradually increased. AO inhibited DNA synthesis and cell mitotic activity in cultured GCT cells and it finally caused inhibition of cell growth. However, the frequencies of G2 arrest cells and binuclear cells were increased. These results suggested that the binuclear cells in GCT may be formed from G2 arrest cells by amitotic nuclear division, but not by mitosis without cytoplasmic division, or by cell fusion.
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PMID:Binuclear cells induced by acridine orange in giant cell tumor of bone. 1106 16

Previous studies from this laboratory have shown that salmon (S) calcitonin (CT)-like immunoreactive peptide (CTI) is synthesized and secreted by the anterior pituitary (AP) gland. These studies also co-localized CTI to gonadotropes, and demonstrated that SCT is a potent inhibitor of lactotrope function. However, the molecular structure of putative gonadotrope-derived CTI that inhibits lactotrope function has not been defined. The present studies cloned CT cDNA (pit-CT cDNA) from a mouse gonadotrope L beta T2 cell line using RT-PCR and rapid amplification of cDNA ends (RACE) techniques. Alignment of nucleotide sequences of pit-CT and mouse CT revealed greater than 99% homology between the sequences. The pit-CT cDNA was ligated into a mammalian expression vector, and the construct was transfected into L beta T2 cells. Two stable transfectant cell lines (CT.U6/A and B) were obtained by selection in G418. Subsequent S1-nuclease protection assay and immunocytochemistry results have shown that: (1) pit-CT peptide expressed by CT.U6 cell lines immunoreacted with GCT1-anti-SCT serum; (2) secretions of CT.U6 cells inhibited prolactin (PRL) release, PRL mRNA abundance and DNA synthesis of PRL-secreting GGH3 cells; and (3) CT.U6-induced inhibition was abolished by GCT1-anti-SCT serum. The studies also generated a riboprobe from the cloned pit-CT cDNA, and localized CT mRNA expression in gonadotropes of rat AP gland by in situ hybridization histochemistry. These results demonstrate that pit-CT mRNA is closely homologous to mouse CT mRNA; it is expressed by gonadotropes of the rat AP gland, and the peptide may significantly affect lactotrope function by inhibiting PRL release and cell proliferation.
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PMID:Calcitonin is expressed in gonadotropes of the anterior pituitary gland: its possible role in paracrine regulation of lactotrope function. 1169 41