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Temozolomide induced c-Myc-mediated apoptosis via Akt signalling in MGMT expressing glioblastoma cells (Articolo in rivista)

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Temozolomide induced c-Myc-mediated apoptosis via Akt signalling in MGMT expressing glioblastoma cells (Articolo in rivista) (literal)

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De Salvo M.1, Maresca G.3, D'agnano I.3, Marchese R.1, Stigliano A.1,2, Gagliassi R.4, Brunetti E.1, Raza G.H.5, De Paula U.5, Bucci B.1 (2011)
Temozolomide induced c-Myc-mediated apoptosis via Akt signalling in MGMT expressing glioblastoma cells
in International journal of radiation biology (Print)
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De Salvo M.1, Maresca G.3, D'agnano I.3, Marchese R.1, Stigliano A.1,2, Gagliassi R.4, Brunetti E.1, Raza G.H.5, De Paula U.5, Bucci B.1 (literal)

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(*) L'INMM è stato soppresso il 12/1/2011 con provvedimento prot. n. 0002122 ed è confluito nell'IBCN costituito il 21/12/2010 con provvedimento prot. n. 0091899. (literal)

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1 - Centro Ricerca S. Pietro, Fatebenefratelli Hospital, 2 - CNR Istituto di Neurobiologia e Medicina Molecolare (*), Ebri, 3 - Cattedra di Endocrinologia, II Facoltà di Medicina, Università \"La Sapienza\", 4 - Laboratorio Analisi Sandro Pertini Hospital, 5 - U.O. di Radioterapia Oncologica S. Pietro, Fatebenefratelli Hospital, Rome, Italy Read More: http://informahealthcare.com/doi/abs/10.3109/09553002.2011.556173 (literal)

Titolo

Temozolomide induced c-Myc-mediated apoptosis via Akt signalling in MGMT expressing glioblastoma cells (literal)

Abstract

PURPOSE: We investigated the molecular mechanisms underlying the cytotoxic effect of Temozolomide (TMZ) in both O(6)-methylguanine-DNA methyl transferase (MGMT) depleted as well as undepleted glioblastoma cell lines. Since TMZ is used in clinics in combination with radiotherapy, we also studied the effects of TMZ in combination with ionising radiation (IR). METHODS: Cell colony-forming ability was measured using a clonogenic assay. Cell cycle analysis and apoptosis were evaluated by Flow Cytometry (FCM). Proteins involved in cell cycle control were detected by Western blot and co-immunoprecipitation assays. RESULTS: Our data showed that TMZ, independent of MGMT expression, inhibited glioblastoma cell growth via an irreversible G(2) block in MGMT depleted cells or the induction of apoptosis in MGMT normal expressing cells. When TMZ was administered in combination with IR, apoptosis was greater than observed with either agent separately. This TMZ-induced apoptosis in the MGMT expressing cells occurred through Akt/Glycogen-Synthase-Kinase-3ß (GSK3ß) signalling and was mediated by Myelocytomatosis (c-Myc) oncoprotein. Indeed, TMZ phosphorylated/activated Akt led to phosphorylation/inactivation of GSK3ß which resulted in the stabilisation of c-Myc protein and subsequent modulation of the c-Myc target genes involved in the apoptotic processes. CONCLUSION: C-Myc expression could be considered a good indicator of TMZ effectiveness. (literal)

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