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Abstract
Neuroblastoma (NB) is the most common pediatric tumor and is currently treated by several types of therapies including chemotherapies, such as bortezomib treatment. However, resistance to bortezomib is frequently observed by mechanisms that remain to be deciphered. Bortezomib treatment leads to caspase activation and aggresome formation. Using models of patients-derived NB cell lines with different levels of sensitivity to bortezomib, we show that the activated form of caspase 3 accumulates within aggresomes of NB resistant cells leading to an impairment of bortezomib-induced apoptosis and increased cell survival. Our findings unveil a new mechanism of resistance to chemotherapy based on an altered subcellular distribution of the executioner caspase 3. This mechanism could explain the resistance developed in NB patients treated with bortezomib, emphasizing the potential of drugs targeting aggresomes.
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Details
1 Univ Lyon, Université Claude Bernard Lyon 1, INSERM U1052, CNRS UMR5286, Centre Léon Bérard, Cancer Research Center of Lyon, Lyon, France (GRID:grid.462282.8) (ISNI:0000 0004 0384 0005)
2 Department of Translational Research and Innovation, Centre Léon Bérard, Lyon, France (GRID:grid.418116.b) (ISNI:0000 0001 0200 3174)
3 Univ Lyon, Université Claude Bernard Lyon 1, INSERM U1052, CNRS UMR5286, Centre Léon Bérard, Cancer Research Center of Lyon, Lyon, France (GRID:grid.462282.8) (ISNI:0000 0004 0384 0005); Institut Convergence PLAsCAN, Lyon Cedex 08, France (GRID:grid.462282.8)
4 Univ Lyon, Université Claude Bernard Lyon 1, INSERM U1052, CNRS UMR5286, Centre Léon Bérard, Cancer Research Center of Lyon, Lyon, France (GRID:grid.462282.8) (ISNI:0000 0004 0384 0005); Institut Convergence PLAsCAN, Lyon Cedex 08, France (GRID:grid.462282.8); DevWeCan Labex Laboratory, Lyon Cedex 08, France (GRID:grid.462282.8)