Na+/K+ ATPase activity promotes invasion of endocrine resistant breast cancer cells

PLoS One. 2018 Mar 28;13(3):e0193779. doi: 10.1371/journal.pone.0193779. eCollection 2018.

Abstract

Background: The Na+/K+-ATPase (NKP) is an important ion transporter also involved in signal transduction. Its expression profile is altered in various tumours including that of the breast. We studied the effect of inhibiting NKP activity in non-tumorigenic breast cell line and in estrogen receptor positive and negative breast cancer cells.

Methods: Expression and localization of NKP and downstream signaling molecules were determined by RT-PCR, western blotting and immunofluorescence. Cell proliferation, apoptosis and cell cycle stage were determined using MTT, annexin V and flow cytometry. Cell motility and invasion were determined using wound healing and matrigel assays. Total matrix metalloproteinase (MMP) was determined by a fluorescence-based assay.

Results: NKP was mainly localized on the cell membrane. Its baseline expression and activity were enhanced in breast cancer compared to the non-tumorigenic breast cell line. Ouabain and 3,4,5,6-tetrahydroxyxanthone (TTX) treatment significantly inhibited NKP activity, which significantly reduced cell proliferation, motility, invasion and pH-induced membrane blebbing. EGF stimulation induced internalization of NKP from the cell membrane to the cytoplasm. Ouabain inhibited EGF-induced phosphorylation of Rac/cdc42, profillin, ERK1/2 and P70S6K.

Conclusions: The NKP may offer a novel therapeutic target in breast cancer patients who have developed metastasis, aiming to improve therapeutic outcomes and enhance survival rate.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Antineoplastic Agents / pharmacology
  • Apoptosis / drug effects
  • Apoptosis / physiology
  • Breast Neoplasms / drug therapy
  • Breast Neoplasms / enzymology*
  • Breast Neoplasms / pathology
  • Cell Cycle / drug effects
  • Cell Cycle / physiology
  • Cell Line, Tumor
  • Cell Membrane / drug effects
  • Cell Membrane / enzymology
  • Cell Membrane / pathology
  • Cell Movement / drug effects
  • Cell Movement / physiology*
  • Dose-Response Relationship, Drug
  • Enzyme Inhibitors / pharmacology
  • Epidermal Growth Factor / metabolism
  • Gene Expression / drug effects
  • Humans
  • Hydrogen-Ion Concentration
  • Neoplasm Invasiveness / physiopathology*
  • Ouabain / pharmacology
  • RNA, Messenger / metabolism
  • RNA, Small Interfering
  • Sodium-Potassium-Exchanging ATPase / antagonists & inhibitors
  • Sodium-Potassium-Exchanging ATPase / genetics
  • Sodium-Potassium-Exchanging ATPase / metabolism*
  • Xanthones / pharmacology

Substances

  • 3,4,5,6-tetrahydroxyxanthone
  • Actins
  • Antineoplastic Agents
  • Enzyme Inhibitors
  • RNA, Messenger
  • RNA, Small Interfering
  • Xanthones
  • Ouabain
  • Epidermal Growth Factor
  • Sodium-Potassium-Exchanging ATPase

Grants and funding

This work was supported by Kuwait University Research Sector grant PT01/14 (MAK). Parts of this work were supported by grant SRUL02/13 to the Research Unit for Genomics, Proteomics and Cellomics Studies (OMICS), Kuwait University.