Altered Intracellular Calcium Fluxes in Pancreatic Cancer Induced Diabetes Mellitus: Relevance of the S100A8 N-Terminal Peptide (NT-S100A8)
| Autor: | Filippo Navaglia, Sergio Pedrazzoli, Andrea Padoan, Eliana Greco, Carlo Reggiani, Carlo-Federico Zambon, Anna Valerio, Daniela Basso, Elisa Fadi, Dania Bozzato, Paola Fogar, Mario Plebani, Michele Scorzeto, Eugenio De Carlo, Roberta Seraglia, Stefania Moz |
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| Rok vydání: | 2011 |
| Předmět: |
EXPRESSION
medicine.medical_specialty Physiology medicine.medical_treatment Clinical Biochemistry TEMPORAL ASSOCIATION PROTEIN KAPPA-B INSULIN-SECRETION Calcium in biology ACTIVATION Islets of Langerhans BETA-CELL FUNCTION Internal medicine Cell Line Tumor Insulin Secretion medicine Extracellular Diabetes Mellitus Animals Humans Insulin Calgranulin A Insulinoma Protein kinase B biology Cell growth TUMOR-GROWTH Cell Biology IN-VITRO MASS-SPECTROMETRY medicine.disease Rats Pancreatic Neoplasms Insulin receptor Endocrinology BETA-CELL FUNCTION IN-VITRO INSULIN-SECRETION KAPPA-B TEMPORAL ASSOCIATION MASS-SPECTROMETRY TUMOR-GROWTH PROTEIN ACTIVATION EXPRESSION Cell culture biology.protein Calcium Peptides Signal Transduction |
| Zdroj: | Journal of cellular physiology 226 (2011): 456–468. doi:10.1002/jcp.22355 info:cnr-pdr/source/autori:Basso D.; Greco E.; Padoan A.; Fogar P.; Scorzeto M.; Fadi E.; Bozzato D.; Moz S.; Navaglia F.; Zambon C.; Seraglia R.; De Carlo E.; Valerio A.; Reggiani C.; Pedrazzoli S.; Plebani M./titolo:Altered Intracellular Calcium Fluxes in Pancreatic Cancer Induced Diabetes Mellitus: Relevance of the S100A8 N-Terminal Peptide (NT-S100A8)/doi:10.1002%2Fjcp.22355/rivista:Journal of cellular physiology (Print)/anno:2011/pagina_da:456/pagina_a:468/intervallo_pagine:456–468/volume:226 |
| DOI: | 10.1002/jcp.22355 |
| Popis: | After isolating NT-S100A8 from pancreatic cancer (PC) tissue of diabetic patients, we verified whether this peptide alters PC cell growth and invasion and/or insulin release and [Ca(2+)](i) oscillations of insulin secreting cells and/or insulin signaling. BxPC3, Capan1, MiaPaCa2, Panc1 (PC cell lines) cell growth, and invasion were assessed in the absence or presence of 50, 200, and 500 nM NT-S100A8. In NT-S100A8 stimulated beta-TC6 (insulinoma cell line) culture medium, insulin and [Ca(2+)](i) were measured at 2, 3, 5, 10, 15, 30, and 60 min, and [Ca(2+)](i) oscillations were monitored (epifluorescence) for 3 min. Five hundred nanomolars NT-S100A8 stimulated BxPC3 cell growth only and dose dependently reduced MiaPaCa2 and Panc1 invasion. Five hundred nanomolars NT-S100A8 induced a rapid insulin release and enhanced beta-TC6 [Ca(2+)](i) oscillations after both one (F = 6.05, P < 0.01) and 2 min (F = 7.42, P < 0.01). In the presence of NT-S100A8, [Ca(2+)] in beta-TC6 culture medium significantly decreased with respect to control cells (F = 6.3, P < 0.01). NT-S100A8 did not counteract insulin induced phosphorylation of the insulin receptor. Akt and I kappa B-alpha, but it independently activated Akt and NF-kappa B signaling in PC cells. In conclusion, NT-S100A8 exerts a mild effect on PC cell growth, while it reduces PC cell invasion, possibly by Akt and NF-kappa B signaling, NT-S100A8 enhances [Ca(2+)](i) oscillations and insulin release, probably by inducing Ca(2+) influx from the extracellular space, but it does not interfere with insulin signaling. |
| Databáze: | OpenAIRE |
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