Glucose-dependent insulinotropic polypeptide stimulated insulin release from a tumor-derived β-cell line (βTC3)

1993 ◽  
Vol 71 (12) ◽  
pp. 917-922 ◽  
Author(s):  
Tim J. Kieffer ◽  
C. Bruce Verchere ◽  
Charlene D. Fell ◽  
Zhongxian Huang ◽  
John C. Brown ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Line ◽  
Glucose Concentration ◽  
Tumor Cell Line ◽  
Immunoreactive Insulin ◽  
Dependent Manner ◽  
Β Cell ◽  
Concentration Dependent Manner ◽  
Glucagon Like Peptide ◽  
Stimulation Of

The βTC3 tumor cell line was examined for the presence of functional glucose-dependent insulinotropic polypeptide (GIP) receptors. Increasing amounts of natural porcine GIP decreased the binding of HPLC-purified [125I]GIP to βTC3 cells in a concentration-dependent manner. Displacement of GIP was significant at concentrations as low as 500 pM, and the radioligand was fully displaced at 100 nM. GIP(1–30) produced a displacement of [125I]GIP comparable with that produced by GIP(1–42), and glucagon yielded 20% displacement at a concentration of 1 μM but was without effect at 100 nM. Incubation of βTC3 cells in the presence of glucose concentrations of 2–20 mM yielded a concentration-dependent stimulation of immunoreactive insulin (IRI) release. GIP and glucagon-like peptide-I(7–36) amide (tGLP-I) at concentrations of 1 nM or greater significantly stimulated IRI release in the presence of 2 mM glucose. The threshold glucose concentration for GIP-stimulated IRI release from βTC3 cells was 0.5 mM, and maximal potentiation of IRI release by GIP occurred at 5 mM glucose. Somatostatin significantly inhibited GIP-stimulated IRI release in the presence of 5 mM glucose. It is concluded that βTC3 cells have functional GIP receptors and may provide a useful model for the study of IRI secretion at the cellular level.Key words: insulin, βTC3, glucose-dependent insulinotropic polypeptide.

Stimulation of Ki-ras Ribozyme Activity by RNA Binding Protein, NCp7, in Vitro and in Pancreatic Tumor Cell Line, Capan 1

1994 ◽  
Vol 733 (1 Molecular and) ◽  
pp. 113-121 ◽  
Author(s):  
KARIN MOELLING ◽  
GERD MUELLER ◽  
JENS DANNULL ◽  
CHRISTOPH REUSS ◽  
PETER BEIMLING ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Line ◽  
Pancreatic Tumor ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Tumor Cell Line ◽  
Pancreatic Tumor Cell ◽  
Stimulation Of

scholarly journals Cytostatic and cytotoxic properties of monensic acid and its biometal(II) complexes against human tumor / non-tumor cell lines

2012 ◽  
Vol 10 (5) ◽  
pp. 1464-1474 ◽  
Author(s):  
Radostina Alexandrova ◽  
Tanya Zhivkova ◽  
Marin Alexandrov ◽  
Georgi Miloshev ◽  
Milena Georgieva ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Line ◽  
Cell Lines ◽  
Human Tumor ◽  
Human Cell Line ◽  
Embryonic Cell ◽  
Dependent Manner ◽  
Tumor Cell Lines ◽  
Concentration Dependent Manner ◽  
Thiazolyl Blue Tetrazolium Bromide

AbstractThe anticancer activity of monensic acid (MonH) and its biometal(II) complexes [M(Mon)2(H2O)2](M = Mg, Ca, Mn, Co, Ni, Zn) was evaluated against cultured human permanent cell lines established from glioblastoma multiforme (8MGBA) and cancers of the lung (A549), breast (MCF-7), uterine cervix (HeLa) and liver (HepG2). The viability and proliferation of the non-tumor human embryonic cell line Lep3 was also tested. The investigations were carried out using a thiazolyl blue tetrazolium bromide test, neutral red uptake cytotoxicity assay, crystal violet staining, colony forming method and double staining with acridin orange and propidium iodide. The results obtained reveal that the compounds applied at concentrations of 0.5–25 µg mL−1 for 24–72 h decrease the viability and proliferation of the treated cells in a time- and concentration-dependent manner. The metal(II) complexes studied (especially those of Co(II), Ni(II) and Zn(II)) have been found to express stronger cytotoxic and cytostatic activities than the non-coordinated monensic acid. The non-tumor human cell line showed strong chemosensitivity towards compounds tested comparable to that of cultured human tumor cell lines.

Effect of secretagogues on cytosolic free Ca2+ and insulin release in the hamster clonal β-cell line HIT-T15

1988 ◽  
Vol 1 (1) ◽  
pp. 13-17 ◽  
Author(s):  
S. J. Hughes ◽  
S. J. H. Ashcroft
Keyword(s):  
Protein Kinase ◽  
Cell Line ◽  
Insulin Release ◽  
Glucose Concentration ◽  
Dependent Manner ◽  
Β Cell ◽  
Tetradecanoylphorbol Acetate ◽  
Dependent Protein ◽  
Hit Cells ◽  
Dose Dependent

ABSTRACT We have examined the effect of secretagogues on cytosolic free Ca2+ (Cai) in the hamster clonal β-cell line HIT-T15 using the Ca2+-binding fluorescent indicator Quin 2. Stimulation of HIT cells by glucose increased Cai in a dose-dependent manner; raising the medium glucose concentration from zero to 2 mm increased Cai by 36%, from 89 ± 4 to 121 ± 6 nm (mean ± s.e.m., n = 23). Further raising the medium glucose concentration to 10 mm increased Cai to 139 ± 6 nm. Cai was maximum and plateaued at 4 min after each addition of glucose. Addition of 40 mm K+ to the medium rapidly depolarized the HIT cells and increased Cai to 407 ± 48 nm. The increases in Cai in response to glucose or K+ were blocked by the simultaneous presence of verapamil (50μm). Stimulation by glucose or K+ also increased insulin release in parallel incubations of Quin 2-loaded HIT cells. Carbamylcholine chloride, forskolin or the phorbol ester 12-O-tetradecanoylphorbol acetate had no significant effect on Cai in glucose-stimulated HIT cells monitored 5 min after the addition of each test agent, despite increasing insulin release by 241, 239 and 216% respectively. These data support the hypothesis that potentiators of insulin release which activate cAMP-dependent protein kinase or protein kinase C do not increase Cai but sensitize the secretory mechanism to Ca2+.

Activation of cyclic AMP-dependent protein kinase activity during LPS stimulation of macrophage tumor cell line, J774.1

1981 ◽  
Vol 3 (1) ◽  
pp. 57-66 ◽  
Author(s):  
Hitoshi Kikutani ◽  
Tadamitsu Kishimoto ◽  
Nobuo Sakaguchi ◽  
Yoshio Nishizawa ◽  
Peter Ralph ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Cyclic Amp ◽  
Tumor Cell ◽  
Cell Line ◽  
Kinase Activity ◽  
Tumor Cell Line ◽  
Protein Kinase Activity ◽  
Dependent Protein Kinase ◽  
Dependent Protein ◽  
Stimulation Of

scholarly journals Regulation of immunoreactive-insulin release from a rat cell line (RINm5F)

1983 ◽  
Vol 210 (2) ◽  
pp. 345-352 ◽  
Author(s):  
G A Praz ◽  
P A Halban ◽  
C B Wollheim ◽  
B Blondel ◽  
A J Strauss ◽  
...  
Keyword(s):  
Cell Line ◽  
Insulin Release ◽  
Insulin Content ◽  
Immunoreactive Insulin ◽  
Dependent Manner ◽  
Rinm5f Cells ◽  
Bicarbonate Buffer ◽  
Delta Cells ◽  
Dose Dependent ◽  
Stimulation Of

1. An insulin-producing cell line, RINm5F, derived from a rat insulinoma was studied. 2. The cellular content of immunoreactive insulin was 0.19 pg/cell, which represents approx. 1% of the insulin content of native rat beta-cells, whereas that of immunoreactive glucagon and somatostatin was five to six orders of magnitude less than that of native alpha- or delta-cells respectively. 3. RINm5F cells released 7-12% of their cellular immunoreactive-insulin content at 2.8 mM-glucose during 60 min in Krebs-Ringer bicarbonate buffer. 4. Glucose utilization was increased by raising glucose from 2.8 to 16.7 mM. There was, however, no stimulation of immunoreactive-insulin release even when glucose was increased from 2.8 to 33.4 mM. A small stimulation of release was, however, found when glucose was raised from 0 to 2.8 mM. 5. Glyceraldehyde stimulated the release of immunoreactive insulin in a dose-dependent manner. 6. At 20 mM, leucine or arginine stimulated release at 2.8 mM-glucose. 7. Raising intracellular cyclic AMP by glucagon or 3-isobutyl-1-methylxanthine stimulated release at 2.8 mM-glucose with no additional stimulation at 16.7 mM-glucose. 8. Stimulation of immunoreactive-insulin release by K+ was dose-related between 2 and 30 mM. Another depolarizing agent, ouabain, also stimulated release. 9. Adrenaline (epinephrine) inhibited both basal (2.8 mM-glucose) release and that stimulated by 30 mM-K+. 10. Raising Ca2+ from 1 to 3 mM stimulated immunoreactive-insulin release, whereas a decrease from 1 to 0.3 or to 0.1 mM-Ca2+ lowered the release. 11. These findings could reflect a relatively specific impairment in glucose handling by RINm5F cells, contrasting with the preserved response to other modulators of insulin release.

Inductive Effect of Human Recombinant IL-1 on Differentiation of a Macrophage-Like Tumor Cell Line

1988 ◽  
Vol 2 (2) ◽  
pp. 372-375 ◽  
Author(s):  
S. Hanazawa ◽  
S. Amano ◽  
C. Hanaizumi ◽  
K. Hirose ◽  
Y. Ohmori ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Line ◽  
Inductive Effect ◽  
Interleukin 1 ◽  
Tumor Cell Line ◽  
Receptor Expression ◽  
Local Factor ◽  
Dose Dependent Fashion ◽  
Dose Dependent ◽  
Stimulation Of

We used the macrophage-like tumor cell line P388D1 to test whether interleukin-1 (IL-1) stimulate differentiation of osteoclast-like progenitors. Recombinant human interleukin-1 (rhIL-1) alpha inhit ited cell growth in a dose-dependent fashion. Incubation of the cells with rhIL-1 alpha resulted in adherence stimulation of non-specific esterase activity, and increased Fc receptor expression. These results suggest th possibility that IL-1 may be involved in the differentiation of osteoclast progenitors and thus may be an irr portant local factor in the mechanism of bone resorption.

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