Literature DB >> 18323016

The sodium pump alpha1 subunit as a potential target to combat apoptosis-resistant glioblastomas.

Florence Lefranc1, Robert Kiss.   

Abstract

PURPOSE: To review the involvement of the ion transporter Na+/K+-ATPase (NaK) in the migration and proliferation of glioma cells. Preliminary studies indicate that NaK alpha1 subunits seem to be upregulated in a proportion of glioblastomas but not in normal brain tissues.
DESIGN: The present review focuses on (1) the natural resistance of migrating malignant glioma cells to apoptosis, (2) autophagic cell death as an alternative to combat malignant gliomas, (3) the fact that reducing the levels of malignant glioma cell motility can restore proapoptotic drug sensitivity,and (4) on the observation that inhibiting the NaK activity reduces both glioma cell proliferation and migration.
RESULTS: The natural ligands of the NaK are the cardiotonic steroids. A hemisynthetic derivative of 2"-oxovoruscharin (UNBS1450), a novel cardenolide, displays unique structural features, making its binding affinity to NaK alpha subunits (including alpha1) 10 to 100 times higher than that of other cardenolides. UNBS1450 markedly decreases intracellular ATP concentration in glioma cells, disorganizes the actin cytoskeleton, and leads to autophagic cell death in NaK alpha1 over-expressing glioma cells.
CONCLUSIONS: Glioblastoma patients who do not respond to chemotherapy and whose tumors over-express NaK alpha1 subunits could benefit from a treatment using ligands with marked binding affinity for the NaK alpha1 subunit.

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Year:  2008        PMID: 18323016      PMCID: PMC2259449          DOI: 10.1593/neo.07928

Source DB:  PubMed          Journal:  Neoplasia        ISSN: 1476-5586            Impact factor:   5.715


  78 in total

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Authors:  Christiane B Knobbe; Guido Reifenberger
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Review 4.  Na+-K+--ATPase-mediated signal transduction: from protein interaction to cellular function.

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Journal:  Mol Interv       Date:  2003-05

5.  Role of autophagy in temozolomide-induced cytotoxicity for malignant glioma cells.

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Journal:  Cell Death Differ       Date:  2004-04       Impact factor: 15.828

6.  Inhibition of DNA repair for sensitizing resistant glioma cells to temozolomide.

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9.  Migrating glioma cells activate the PI3-K pathway and display decreased susceptibility to apoptosis.

Authors:  Anna M Joy; Christian E Beaudry; Nhan L Tran; Francisco A Ponce; David R Holz; Tim Demuth; Michael E Berens
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Review 10.  Malignant gliomas: perverting glutamate and ion homeostasis for selective advantage.

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2.  Lanatoside C sensitizes glioblastoma cells to tumor necrosis factor-related apoptosis-inducing ligand and induces an alternative cell death pathway.

Authors:  Christian E Badr; Thomas Wurdinger; Jonas Nilsson; Johanna M Niers; Michael Whalen; Alexei Degterev; Bakhos A Tannous
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4.  The anticancer drug perillyl alcohol is a Na/K-ATPase inhibitor.

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5.  The influence of oxo-bridged binuclear gold(III) complexes on Na/K-ATPase activity: a joint experimental and theoretical approach.

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6.  The War on Cancer rages on.

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7.  The predictive potential of hyponatremia for glioblastoma patient survival.

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8.  Combining bevacizumab with temozolomide increases the antitumor efficacy of temozolomide in a human glioblastoma orthotopic xenograft model.

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9.  Neoplasia: the second decade.

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10.  Cardiac glycosides induce cell death in human cells by inhibiting general protein synthesis.

Authors:  Andrea Perne; Markus K Muellner; Magdalena Steinrueck; Nils Craig-Mueller; Julia Mayerhofer; Ilse Schwarzinger; Mathew Sloane; Iris Z Uras; Gregor Hoermann; Sebastian M B Nijman; Matthias Mayerhofer
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