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Breast cancer-derived K172N, D301V mutations abolish Na+/H+ exchanger regulatory factor 1 inhibition of platelet-derived growth factor receptor signaling.

Abstract
Na(+)/H(+) exchanger regulatory factor 1 (NHERF1) is a scaffold protein known to interact with a number of cancer-related proteins. nherf1 Mutations (K172N and D301V) were recently identified in breast cancer cells. To investigate the functional properties of NHERF1, wild-type and cancer-derived nherf1 mutations were stably expressed in SKMES-1 cells respectively. NHERF1-wt overexpression suppressed the cellular malignant phenotypes, including proliferation, migration, and invasion. nherf1 Mutations (K172N and D301V) caused complete or partial loss of NHERF1 functions by affecting the PTEN/NHERF1/PDGFRβ complex formation, inactivating NHERF1 inhibition of PDGF-induced AKT and ERK activation, and attenuating the tumor-suppressor effects of NHERF1-wt. These results further demonstrated the functional consequences of breast cancer-derived nherf1 mutations (K172N and D301V), and suggested the causal role of NHERF1 in tumor development and progression.
AuthorsShan Cheng, Yang Li, Ying Yang, Duiping Feng, Longyan Yang, Qian Ma, Shuai Zheng, Ran Meng, Shuhui Wang, Songlin Wang, Wen G Jiang, Junqi He
JournalFEBS letters (FEBS Lett) Vol. 587 Issue 20 Pg. 3289-95 (Oct 11 2013) ISSN: 1873-3468 [Electronic] England
PMID24012959 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2013 Federation of European Biochemical Societies. All rights reserved.
Chemical References
  • Phosphoproteins
  • Sodium-Hydrogen Exchangers
  • sodium-hydrogen exchanger regulatory factor
  • Receptor, Platelet-Derived Growth Factor beta
  • PTEN Phosphohydrolase
  • PTEN protein, human
Topics
  • Animals
  • Breast Neoplasms (genetics, metabolism)
  • COS Cells
  • Cell Line, Tumor
  • Cell Proliferation
  • Chlorocebus aethiops
  • Female
  • Humans
  • Mutation
  • PTEN Phosphohydrolase (genetics, metabolism)
  • Phosphoproteins (genetics, metabolism)
  • Protein Binding
  • Receptor, Platelet-Derived Growth Factor beta (genetics, metabolism)
  • Sodium-Hydrogen Exchangers (genetics, metabolism)

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