000070917 001__ 70917
000070917 005__ 20191126134634.0
000070917 0247_ $$2doi$$a10.3390/ijms19051449
000070917 0248_ $$2sideral$$a106456
000070917 037__ $$aART-2018-106456
000070917 041__ $$aeng
000070917 100__ $$aGallego-Lleyda, A.$$uUniversidad de Zaragoza
000070917 245__ $$aLipid nanoparticles decorated with TNF-related aptosis-inducing ligand (TRAIL) are more cytotoxic than soluble recombinant TRAIL in sarcoma
000070917 260__ $$c2018
000070917 5060_ $$aAccess copy available to the general public$$fUnrestricted
000070917 5203_ $$aSarcomas are rare and heterogeneous cancers classically associated with a poor outcome. Sarcomas are 1% of the cancer but recent estimations indicate that sarcomas account for 2% of the estimated cancer-related deaths. Traditional treatment with surgery, radiotherapy, and chemotherapy has improved the outcome for some types of sarcomas. However, novel therapeutic strategies to treat sarcomas are necessary. TNF-related apoptosis-inducing ligand (TRAIL) is a death ligand initially described as capable of inducing apoptosis on tumor cell while sparing normal cells. Only few clinical trials have used TRAIL-based treatments in sarcoma, but they show only low or moderate efficacy of TRAIL. Consequently, novel TRAIL formulations with an improved TRAIL bioactivity are necessary. Our group has developed a novel TRAIL formulation based on tethering this death ligand on a lipid nanoparticle surface (LUV-TRAIL) resembling the physiological secretion of TRAIL as a trasmembrane protein inserted into the membrane of exosomes. We have already demonstrated that LUV-TRAIL shows an improved cytotoxic activity when compared to soluble recombinant TRAIL both in hematological malignancies and epithelial-derived cancers. In the present study, we have tested LUV-TRAIL in several human sarcoma tumor cell lines with different sensitivity to soluble recombinant TRAIL, finding that LUV-TRAIL was more efficient than soluble recombinant TRAIL. Moreover, combined treatment of LUV-TRAIL with distinct drugs proved to be especially effective, sensitizing even more resistant cell lines to TRAIL.
000070917 536__ $$9info:eu-repo/grantAgreement/ES/ISCIII/PI16-00526
000070917 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttp://creativecommons.org/licenses/by/3.0/es/
000070917 590__ $$a4.183$$b2018
000070917 591__ $$aCHEMISTRY, MULTIDISCIPLINARY$$b45 / 172 = 0.262$$c2018$$dQ2$$eT1
000070917 591__ $$aBIOCHEMISTRY & MOLECULAR BIOLOGY$$b77 / 294 = 0.262$$c2018$$dQ2$$eT1
000070917 592__ $$a1.312$$b2018
000070917 593__ $$aCatalysis$$c2018$$dQ1
000070917 593__ $$aComputer Science Applications$$c2018$$dQ1
000070917 593__ $$aInorganic Chemistry$$c2018$$dQ1
000070917 593__ $$aSpectroscopy$$c2018$$dQ1
000070917 593__ $$aMolecular Biology$$c2018$$dQ1
000070917 593__ $$aOrganic Chemistry$$c2018$$dQ1
000070917 593__ $$aPhysical and Theoretical Chemistry$$c2018$$dQ1
000070917 593__ $$aMedicine (miscellaneous)$$c2018$$dQ1
000070917 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000070917 700__ $$aDe Miguel, D.
000070917 700__ $$0(orcid)0000-0002-5175-8394$$aAnel, A.$$uUniversidad de Zaragoza
000070917 700__ $$aMartinez-Lostao, L.
000070917 7102_ $$11002$$2060$$aUniversidad de Zaragoza$$bDpto. Bioq.Biolog.Mol. Celular$$cÁrea Bioquímica y Biolog.Mole.
000070917 7102_ $$11002$$2050$$aUniversidad de Zaragoza$$bDpto. Bioq.Biolog.Mol. Celular$$cÁrea Biología Celular
000070917 773__ $$g19, 5 (2018), 1449 [18 pp]$$pInt. j. mol. sci.$$tInternational Journal of Molecular Sciences$$x1661-6596
000070917 8564_ $$s932838$$uhttps://zaguan.unizar.es/record/70917/files/texto_completo.pdf$$yVersión publicada
000070917 8564_ $$s109102$$uhttps://zaguan.unizar.es/record/70917/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000070917 909CO $$ooai:zaguan.unizar.es:70917$$particulos$$pdriver
000070917 951__ $$a2019-11-26-13:42:51
000070917 980__ $$aARTICLE