Differential effects of two-pore channel protein 1 and 2 silencing in MDA-MB-468 breast cancer cells

Jahidin AH 1 , Stewart TA 2 , Thompson EW 3 , Roberts-Thomson SJ 4 , Monteith GR 5

Affiliations 

  • 1 School of Pharmacy, The University of Queensland, Brisbane, Queensland, Australia; Faculty of Pharmacy, Universiti Teknologi MARA, Puncak Alam Campus, Selangor, Malaysia. Electronic address: aisya735@puncakalam.uitm.edu.my
  • 2 School of Pharmacy, The University of Queensland, Brisbane, Queensland, Australia. Electronic address: teneale.stewart@uq.edu.au
  • 3 Institute of Health and Biomedical Innovation and School of Biomedical Sciences, Queensland University of Technology, Kelvin Grove, Queensland, Australia; Queensland University of Technology Translational Research Institute, Brisbane, Queensland, Australia. Electronic address: e2.thompson@qut.edu.au
  • 4 School of Pharmacy, The University of Queensland, Brisbane, Queensland, Australia. Electronic address: sarahrt@uq.edu.au
  • 5 School of Pharmacy, The University of Queensland, Brisbane, Queensland, Australia; Mater Research, Translational Research Institute, The University of Queensland, Brisbane, Queensland, Australia; The University of Queensland, Translational Research Institute, Brisbane, Queensland, Australia. Electronic address: gregm@uq.edu.au
Biochem Biophys Res Commun, 2016 Sep 02;477(4):731-736.
PMID: 27353380 DOI: 10.1016/j.bbrc.2016.06.127

Abstract

Two-pore channel proteins, TPC1 and TPC2, are calcium permeable ion channels found localized to the membranes of endolysosomal calcium stores. There is increasing interest in the role of TPC-mediated intracellular signaling in various pathologies; however their role in breast cancer has not been extensively evaluated. TPC1 and TPC2 mRNA was present in all non-tumorigenic and tumorigenic breast cell lines assessed. Silencing of TPC2 but not TPC1 attenuated epidermal growth factor-induced vimentin expression in MDA-MB-468 breast cancer cells. This effect was not due to a general inhibition of epithelial to mesenchymal transition (EMT) as TPC2 silencing had no effect on epidermal growth factor (EGF)-induced changes on E-cadherin expression. TPC1 and TPC2 were also shown to differentially regulate cyclopiazonic acid (CPA)-mediated changes in cytosolic free Ca(2+). These findings indicate potential differential regulation of signaling processes by TPC1 and TPC2 in breast cancer cells.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.

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