Cell death induced in a human glioblastoma cell line by p(65)+Be neutrons combined with cisplatin

Benzina, Sami; Fischer, Barbara; Miternique-Grosse, Anne; Dufour, Patrick; Denis, Jean‐Marc; Bergerat, Jean‐Pierre; Gueulette, John; Bischoff, Pierre

doi:10.1016/j.lfs.2006.01.037

Cited by 10 publications

(7 citation statements)

References 28 publications

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“…Benzina et al (21) reported that fast neutrons combined with cisplatin induced a senescence-like cell cycle arrest in glioblastoma cells. However, this phenomenon has not yet been described in response to carbon ions.…”

Section: Discussionmentioning

confidence: 99%

Different Mechanisms of Cell Death in Radiosensitive and Radioresistant P53 Mutated Head and Neck Squamous Cell Carcinoma Cell Lines Exposed to Carbon Ions and X-Rays

Maalouf

Alphonse

Colliaux

et al. 2009

International Journal of Radiation Oncology*Biology*Physics

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Section: Discussionmentioning

confidence: 99%

Different Mechanisms of Cell Death in Radiosensitive and Radioresistant P53 Mutated Head and Neck Squamous Cell Carcinoma Cell Lines Exposed to Carbon Ions and X-Rays

Maalouf

Alphonse

Colliaux

et al. 2009

International Journal of Radiation Oncology*Biology*Physics

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“…Alternatively, apoptosis was also measured by propidium iodide staining followed by flow cytometry as previously described (21). Caspase 3/7 activity was measured by using the Caspase-Glo 3/7 Assay (Promega).…”

Section: Apoptosismentioning

confidence: 99%

A Sensitized RNA Interference Screen Identifies a Novel Role for the PI3K p110γ Isoform in Medulloblastoma Cell Proliferation and Chemoresistance

Guerreiro

Fattet

Kulesza

et al. 2011

Molecular Cancer Research

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Medulloblastoma is the most common malignant brain tumor in children and is associated with a poor outcome. We were interested in gaining further insight into the potential of targeting the human kinome as a novel approach to sensitize medulloblastoma to chemotherapeutic agents. A library of small interfering RNA (siRNA) was used to downregulate the known human protein and lipid kinases in medulloblastoma cell lines. The analysis of cell proliferation, in the presence or absence of a low dose of cisplatin after siRNA transfection, identified new protein and lipid kinases involved in medulloblastoma chemoresistance. PLK1 (polo-like kinase 1) was identified as a kinase involved in proliferation in medulloblastoma cell lines. Moreover, a set of 6 genes comprising ATR, LYK5, MPP2, PIK3CG, PIK4CA, and WNK4 were identified as contributing to both cell proliferation and resistance to cisplatin treatment in medulloblastoma cells. An analysis of the expression of the 6 target genes in primary medulloblastoma tumor samples and cell lines revealed overexpression of LYK5 and PIK3CG. The results of the siRNA screen were validated by target inhibition with specific pharmacological inhibitors. A pharmacological inhibitor of p110g (encoded by PIK3CG) impaired cell proliferation in medulloblastoma cell lines and sensitized the cells to cisplatin treatment. Together, our data show that the p110g phosphoinositide 3-kinase isoform is a novel target for combinatorial therapies in medulloblastoma. Mol Cancer Res; 9(7); 925-35. '2011 AACR.

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“…Alternatively, the Cell Death detection ELISA method (Roche Diagnostics) was used. Apoptosis was also measured by propidium iodide staining followed by flow cytometry as described previously (30).…”

Section: Translational Relevancementioning

confidence: 99%

Targeting the PI3K p110α Isoform Inhibits Medulloblastoma Proliferation, Chemoresistance, and Migration

Guerreiro

Fattet

Fischer

et al. 2008

Clinical Cancer Research

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Purpose: The phosphoinositide 3-kinase (PI3K)/Akt pathway is frequently activated in human cancer and plays a crucial role in medulloblastoma biology. We were interested in gaining further insight into the potential of targeting PI3K/Akt signaling as a novel antiproliferative approach in medulloblastoma. Experimental Design: The expression pattern and functions of class I A PI3K isoforms were investigated in medulloblastoma tumour samples and cell lines. Effects on cell survival and downstream signaling were analyzed following down-regulation of p110a, p110h, or p110y by means of RNA interference or inhibition with isoform-specific PI3K inhibitors. Results: Overexpression of the catalytic p110a isoform was detected in a panel of primary medulloblastoma samples and cell lines compared with normal brain tissue. Down-regulation of p110a expression by RNA interference impaired the growth of medulloblastoma cells, induced apoptosis, and led to decreased migratory capacity of the cells.This effect was selective, because RNA interference targeting of p110h or p110y did not result in a comparable impairment of DAOY cell survival. Isoform-specific p110ainhibitors also impaired medulloblastoma cell proliferation and sensitized the cells to chemotherapy. Medulloblastoma cells treated with p110a inhibitors further displayed reduced activation of Akt and the ribosomal protein S6 kinase in response to stimulation with hepatocyte growth factor and insulin-like growth factor-I. Conclusions:Together, our data reveal a novel function of p110a in medulloblastoma growth and survival.

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Cell death induced in a human glioblastoma cell line by p(65)+Be neutrons combined with cisplatin

Cited by 10 publications

References 28 publications

Different Mechanisms of Cell Death in Radiosensitive and Radioresistant P53 Mutated Head and Neck Squamous Cell Carcinoma Cell Lines Exposed to Carbon Ions and X-Rays

Different Mechanisms of Cell Death in Radiosensitive and Radioresistant P53 Mutated Head and Neck Squamous Cell Carcinoma Cell Lines Exposed to Carbon Ions and X-Rays

A Sensitized RNA Interference Screen Identifies a Novel Role for the PI3K p110γ Isoform in Medulloblastoma Cell Proliferation and Chemoresistance

Targeting the PI3K p110α Isoform Inhibits Medulloblastoma Proliferation, Chemoresistance, and Migration

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