Acute cytotoxicity of MIRA-1/NSC19630, a mutant p53-reactivating small molecule, against human normal and cancer cells via a caspase-9-dependent apoptosis

Acute cytotoxicity of MIRA-1/NSC19630, a mutant p53-reactivating small molecule, against human normal and cancer cells via a caspase-9-dependent apoptosis

Highlights • Aim: toxicological evaluation of Mira-1, first described as a mutant P53-reactivating agent. • Acute cytotoxicity of Mira-1 against human normal epithelial and primary mesenchymal cells. • Mira-1 cytotoxicity is restricted to actively proliferating cells. • Acute cytotoxicity of Mira-1...

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Veröffentlicht in:Cancer letters 2015-04, Vol.359 (2), p.211-217
Hauptverfasser: Bou-Hanna, Chantal, Jarry, Anne, Lode, Laurence, Schmitz, Ingo, Schulze-Osthoff, Klaus, Kury, Sébastien, Bezieau, Stéphane, Mosnier, Jean-François, Laboisse, Christian L
Format: Artikel
Sprache:eng
Schlagworte:
Aged
Antineoplastic Agents - pharmacology
Apoptosis
Apoptosis - drug effects
Cancer
Cancer cell lines
Cancer therapies
Caspase 9 - physiology
Cell cycle
Cell Line, Tumor
Cell Survival
Chemotherapy
Colonic Neoplasms - drug therapy
Colonic Neoplasms - pathology
Cytotoxicity
Drug dosages
Drug Screening Assays, Antitumor
Explant culture
Female
Fibroblasts - drug effects
Fibroblasts - physiology
Growth phase
Hematology, Oncology and Palliative Medicine
Humans
Kinases
Life Sciences
Male
Maleimides - pharmacology
Medical research
Middle Aged
Molecular weight
Multiple myeloma
Mutation
Primary normal cells
Toxicology
Tumor Suppressor Protein p53 - genetics
Tumor Suppressor Protein p53 - metabolism
Tumors
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Zusammenfassung:Highlights • Aim: toxicological evaluation of Mira-1, first described as a mutant P53-reactivating agent. • Acute cytotoxicity of Mira-1 against human normal epithelial and primary mesenchymal cells. • Mira-1 cytotoxicity is restricted to actively proliferating cells. • Acute cytotoxicity of Mira-1 against cancer cell lines is independent from their TP53 status. • The mira-1 cytotoxicity is mediated by a caspase-9-dependent apoptotic effect.
ISSN:0304-3835
1872-7980
DOI:10.1016/j.canlet.2015.01.014