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Lanatoside C sensitizes glioblastoma cells to tumor necrosis factor-related apoptosis-inducing ligand and induces an alternative cell death pathway.
Neuro-oncology Research Group, Department of Neurosurgery, VU University Medical Center, Amsterdam, Netherlands.
Vise andre og tillknytning
2011 (engelsk)Inngår i: Neuro-Oncology, ISSN 1522-8517, E-ISSN 1523-5866, Vol. 13, nr 11, 1213-1224 s.Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Human glioblastoma (GBM) cells are notorious for their resistance to apoptosis-inducing therapeutics. We have identified lanatoside C as a sensitizer of GBM cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced cell death partly by upregulation of the death receptor 5. We show that lanatoside C sensitizes GBM cells to TRAIL-induced apoptosis in a GBM xenograft model in vivo. Lanatoside C on its own serves as a therapeutic agent against GBM by activating a caspase-independent cell death pathway. Cells treated with lanatoside C showed necrotic cell morphology with absence of caspase activation, low mitochondrial membrane potential, and early intracellular ATP depletion. In conclusion, lanatoside C sensitizes GBM cells to TRAIL-induced cell death and mitigates apoptosis resistance of glioblastoma cells by inducing an alternative cell death pathway. To our knowledge, this is one of the first examples of use of caspase-independent cell death inducers to trigger tumor regression in vivo. Activation of such mechanism may be a useful strategy to counter resistance of cancer cells to apoptosis.

sted, utgiver, år, opplag, sider
2011. Vol. 13, nr 11, 1213-1224 s.
Emneord [en]
cardiac glycoside, glioblastoma, lanatoside, C, non-apoptotic cell death, TRAIL
HSV kategori
Identifikatorer
URN: urn:nbn:se:umu:diva-55701DOI: 10.1093/neuonc/nor067PubMedID: 21757445OAI: oai:DiVA.org:umu-55701DiVA: diva2:528761
Tilgjengelig fra: 2012-05-28 Laget: 2012-05-28 Sist oppdatert: 2017-12-07bibliografisk kontrollert

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