Filamin-a is required to mediate SST2 effects in pancreatic neuroendocrine tumours

Research output: Contribution to journalArticle

Abstract

Somatostatin receptor type 2 (SST2) is the main pharmacological target of somatostatin (SS) analogues widely used in patients with pancreatic neuroendocrine tumours (P-NETs), this treatment being ineffective in a subset of patients. Since it has been demonstrated that Filamin A (FLNA) is involved in mediating GPCR expression, membrane anchoring and signalling, we investigated the role of this cytoskeleton protein in SST2 expression and signalling, angiogenesis, cell adhesion and cell migration in human P-NETs and in QGP1 cell line. We demonstrated that FLNA silencing was not able to affect SST2 expression in P-NET cells in basal conditions. Conversely, a significant reduction in SST2 expression (-43±21%, P

Original languageEnglish
Pages (from-to)181-190
Number of pages10
JournalEndocrine-Related Cancer
Volume23
Issue number3
DOIs
Publication statusPublished - Mar 1 2016

Fingerprint

Filamins
Neuroendocrine Tumors
Neuroendocrine Cells
Somatostatin
Cytoskeleton
Cell Adhesion
Cell Movement
Pharmacology
Cell Line
Membranes
somatostatin receptor 2
Proteins

Keywords

  • Filamin A
  • Neuroendocrine tumours
  • Somatostatin
  • Somatostatin receptor type 2

ASJC Scopus subject areas

  • Endocrinology
  • Oncology
  • Cancer Research
  • Endocrinology, Diabetes and Metabolism

Cite this

@article{fdef7823964f4de7b7ff5d915bc99413,
title = "Filamin-a is required to mediate SST2 effects in pancreatic neuroendocrine tumours",
abstract = "Somatostatin receptor type 2 (SST2) is the main pharmacological target of somatostatin (SS) analogues widely used in patients with pancreatic neuroendocrine tumours (P-NETs), this treatment being ineffective in a subset of patients. Since it has been demonstrated that Filamin A (FLNA) is involved in mediating GPCR expression, membrane anchoring and signalling, we investigated the role of this cytoskeleton protein in SST2 expression and signalling, angiogenesis, cell adhesion and cell migration in human P-NETs and in QGP1 cell line. We demonstrated that FLNA silencing was not able to affect SST2 expression in P-NET cells in basal conditions. Conversely, a significant reduction in SST2 expression (-43±21{\%}, P",
keywords = "Filamin A, Neuroendocrine tumours, Somatostatin, Somatostatin receptor type 2",
author = "Eleonora Vitali and Valeria Cambiaghi and Alessandro Zerbi and Carlo Carnaghi and Piergiuseppe Colombo and Erika Peverelli and Anna Spada and Giovanna Mantovani and Lania, {Andrea G.}",
year = "2016",
month = "3",
day = "1",
doi = "10.1530/ERC-15-0358",
language = "English",
volume = "23",
pages = "181--190",
journal = "Endocrine-Related Cancer",
issn = "1351-0088",
publisher = "BioScientifica Ltd.",
number = "3",

}

TY - JOUR

T1 - Filamin-a is required to mediate SST2 effects in pancreatic neuroendocrine tumours

AU - Vitali, Eleonora

AU - Cambiaghi, Valeria

AU - Zerbi, Alessandro

AU - Carnaghi, Carlo

AU - Colombo, Piergiuseppe

AU - Peverelli, Erika

AU - Spada, Anna

AU - Mantovani, Giovanna

AU - Lania, Andrea G.

PY - 2016/3/1

Y1 - 2016/3/1

N2 - Somatostatin receptor type 2 (SST2) is the main pharmacological target of somatostatin (SS) analogues widely used in patients with pancreatic neuroendocrine tumours (P-NETs), this treatment being ineffective in a subset of patients. Since it has been demonstrated that Filamin A (FLNA) is involved in mediating GPCR expression, membrane anchoring and signalling, we investigated the role of this cytoskeleton protein in SST2 expression and signalling, angiogenesis, cell adhesion and cell migration in human P-NETs and in QGP1 cell line. We demonstrated that FLNA silencing was not able to affect SST2 expression in P-NET cells in basal conditions. Conversely, a significant reduction in SST2 expression (-43±21%, P

AB - Somatostatin receptor type 2 (SST2) is the main pharmacological target of somatostatin (SS) analogues widely used in patients with pancreatic neuroendocrine tumours (P-NETs), this treatment being ineffective in a subset of patients. Since it has been demonstrated that Filamin A (FLNA) is involved in mediating GPCR expression, membrane anchoring and signalling, we investigated the role of this cytoskeleton protein in SST2 expression and signalling, angiogenesis, cell adhesion and cell migration in human P-NETs and in QGP1 cell line. We demonstrated that FLNA silencing was not able to affect SST2 expression in P-NET cells in basal conditions. Conversely, a significant reduction in SST2 expression (-43±21%, P

KW - Filamin A

KW - Neuroendocrine tumours

KW - Somatostatin

KW - Somatostatin receptor type 2

UR - http://www.scopus.com/inward/record.url?scp=84963959675&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84963959675&partnerID=8YFLogxK

U2 - 10.1530/ERC-15-0358

DO - 10.1530/ERC-15-0358

M3 - Article

AN - SCOPUS:84963959675

VL - 23

SP - 181

EP - 190

JO - Endocrine-Related Cancer

JF - Endocrine-Related Cancer

SN - 1351-0088

IS - 3

ER -