Titre
Kinesin spindle protein SiRNA slows tumor progression.
Type
article
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Périodique
Auteur(s)
Marra, E.
Auteure/Auteur
Palombo, F.
Auteure/Auteur
Ciliberto, G.
Auteure/Auteur
Aurisicchio, L.
Auteure/Auteur
Liens vers les unités
ISSN
1097-4652
Statut éditorial
Publié
Date de publication
2013
Volume
228
Numéro
1
Première page
58
Dernière page/numéro d’article
64
Langue
anglais
Notes
Publication types: Journal ArticlePublication Status: ppublish
Résumé
The kinesin spindle protein (KSP), a member of the kinesin superfamily of microtubule-based motors, plays a critical role in mitosis as it mediates centrosome separation and bipolar spindle assembly and maintenance. Inhibition of KSP function leads to cell cycle arrest at mitosis with the formation of monoastral microtubule arrays, and ultimately, to cell death. Several KSP inhibitors are currently being studied in clinical trials and provide new opportunities for the development of novel anticancer therapeutics. RNA interference (RNAi) may represent a powerful strategy to interfere with key molecular pathways involved in cancer. In this study, we have established an efficient method for intratumoral delivery of siRNA. We evaluated short interfering RNA (siRNA) duplexes targeting luciferase as surrogate marker or KSP sequence. To examine the potential feasibility of RNAi therapy, the siRNA was transfected into pre-established lesions by means of intratumor electro-transfer of RNA therapeutics (IERT). This technology allowed cell permeation of the nucleic acids and to efficiently knock down gene expression, albeit transiently. The KSP-specific siRNA drastically reduced outgrowth of subcutaneous melanoma and ovarian cancer lesions. Our results show that intratumoral electro-transfer of siRNA is feasible and KSP-specific siRNA may provide a novel strategy for therapeutic intervention. J. Cell. Physiol. 228: 58-64, 2013. © 2012 Wiley Periodicals, Inc.
PID Serval
serval:BIB_6042052A8724
PMID
Date de création
2012-11-23T18:39:20.374Z
Date de création dans IRIS
2025-05-20T16:36:52Z