Display Settings:

Format

Send to:

Choose Destination
We are sorry, but NCBI web applications do not support your browser and may not function properly. More information
    Cell Death Differ. 2007 Jul;14(7):1295-304. Epub 2007 May 4.

    Ion channels in death and differentiation of prostate cancer cells.

    Source

    Laboratoire de Physiologie Cellulaire, Equipe labellisée par la Ligue contre le cancer, INSERM U800, Université de Lille 1, Villeneuve d'Ascq F-59650, France. Natacha.Prevarskaya@univ-lille1.fr

    Abstract

    Plasma membrane ion channels contribute to virtually all basic cellular processes, including such crucial ones for maintaining tissue homeostasis as proliferation, differentiation, and apoptosis. Enhanced proliferation, aberrant differentiation, and impaired ability to die are the prime reasons for abnormal tissue growth, which can eventually turn into uncontrolled expansion and invasion, characteristic of cancer. Prostate cancer (PCa) cells express a variety of plasma membrane ion channels. By providing the influx of essential signaling ions, perturbing intracellular ion concentrations, regulating cell volume, and maintaining membrane potential, PCa cells are critically involved in proliferation, differentiation, and apoptosis. PCa cells of varying metastatic ability can be distinguished by their ion channel characteristics. Increased malignancy and invasiveness of androgen-independent PCa cells is generally associated with the shift to a 'more excitable' phenotype of their plasma membrane. This shift is manifested by the appearance of voltage-gated Na(+) and Ca(2+) channels which contribute to their enhanced apoptotic resistance together with downregulated store-operated Ca(2+) influx, altered expression of different K(+) channels and members of the Transient Receptor Potential (TRP) channel family, and strengthened capability for maintaining volume constancy. The present review examines channel types expressed by PCa cells and their involvement in metastatic behaviors.

    PMID:
    17479110
    [PubMed - indexed for MEDLINE]
    Free full text

      Supplemental Content

      Icon for Nature Publishing Group

      Save items

      Recent activity

      Your browsing activity is empty.

      Activity recording is turned off.

      Turn recording back on

      See more...
      Write to the Help Desk