title: Gefitinib inhibits sodium phosphate co-transporter III isoform 1 in a model of human malignant glioma.
abstract: BACKGROUND
  The purpose of the present was to investigate whether the in vitro effects of gefitinib, an EGFR tyrosine kinase inhibitor, may regulate the expression of type III sodium phosphate Na/Pi co-transporters in an in vitro glioma model.
  
  
  METHODS
  Proliferation studies, global native EGFR and phosphorylated EGFR expressions, phosphate transporter type III isoform 1(PiT1) expression and phosphate transport with 99mTc-(V)-DMSA radioligand were performed in G111 (grade II astrocytoma), U-87-MG (grade III astrocytoma) and G152 (grade IV glioblastoma) cells.
  
  
  RESULTS
  Cells treated with gefitinib showed a significant decrease in proliferation in relation to EGFR and p-EGFR expression. Gefitinib also produced a decrease in phosphate transport mediated PIT1 expression at both the RNA and protein levels.
  
  
  CONCLUSIONS
  The link between gefitinib acting on the EGFR and PiT1 regulation in these cancer cell lines was herein shown.
authors.affiliation: Interdisciplinary Laboratory for the Study of Aerosolized Nanoparticles, (LINA) Research Group EA 4624, Jacques Lisfranc Faculty of Medicine, University of Lyon Saint-Etienne, Saint-Etienne, France.
authors.forename: Clementine
authors.initials: C
authors.lastname: Puech
authors.affiliation: Interdisciplinary Laboratory for the Study of Aerosolized Nanoparticles, (LINA) Research Group EA 4624, Jacques Lisfranc Faculty of Medicine, University of Lyon Saint-Etienne, Saint-Etienne, France.
authors.forename: Nathalie
authors.initials: N
authors.lastname: Prevot
authors.affiliation: Interdisciplinary Laboratory for the Study of Aerosolized Nanoparticles, (LINA) Research Group EA 4624, Jacques Lisfranc Faculty of Medicine, University of Lyon Saint-Etienne, Saint-Etienne, France nathalie.perek@univ-st-etienne.fr.
authors.forename: Nathalie
authors.initials: N
authors.lastname: Perek
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D015153:Blotting, Western; D049109:Cell Proliferation / Q000187:drug effects; D004797:Enzyme-Linked Immunosorbent Assay; D066246:ErbB Receptors / Q000235:genetics / Q000378:metabolism*; D000077156:Gefitinib; D005909:Glioblastoma / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D060787:Neoplasm Grading; D010710:Phosphates / Q000378:metabolism; D020033:Protein Isoforms; D011799:Quinazolines / Q000494:pharmacology*; D012333:RNA, Messenger / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D050611:Sodium-Phosphate Cotransporter Proteins, Type III / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism; D014407:Tumor Cells, Cultured
chemical_list: D000970:Antineoplastic Agents; D010710:Phosphates; D020033:Protein Isoforms; D011799:Quinazolines; D012333:RNA, Messenger; D050611:Sodium-Phosphate Cotransporter Proteins, Type III; C512478:EGFR protein, human; D066246:ErbB Receptors; D000077156:Gefitinib
keywords: EGFR signaling; Gefitinib; PiT-1; malignant gliomas