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dc.creatorMojić, Marija
dc.creatorMijatović, Sanja
dc.creatorMaksimović-Ivanić, Danijela
dc.creatorMiljković, Djordje
dc.creatorStošić-Grujičić, Stanislava
dc.creatorStanković, Marija
dc.creatorMangano, Katia
dc.creatorTravali, Salvatore
dc.creatorDonia, Marco
dc.creatorFagone, Paolo
dc.creatorZocca, Mai-Britt
dc.creatorAl-Abed, Yousef
dc.creatorMcCubrey, James A.
dc.creatorNicoletti, Ferdinando
dc.date.accessioned2022-11-15T14:11:40Z
dc.date.available2022-11-15T14:11:40Z
dc.date.issued2012
dc.identifier.issn0026-895X
dc.identifier.urihttps://imagine.imgge.bg.ac.rs/handle/123456789/548
dc.description.abstractWe have examined the influence of the nitric oxide (NO)modified anti-inflammatory drug (S, R)-3-phenyl-4,5-dihydro-5-isoxasole acetic acid (VGX-1027) named GIT-27NO or the NO-modified antiviral drug saquinavir (Saq) named Saq-NO on two colon cancer cell lines, mouse CT26CL25 and human HCT116. The effects of the drugs on cell viability, apoptosis, proliferation, and metastatic potential were analyzed. The release of NO and oxygen and nitrogen species was also determined. The efficacy of the drugs was evaluated in vivo in BALB/c mice injected with CT26CL25 cells. Both agents suppressed the growth of colon cancer cells in vitro and reduced tumor volume in syngeneic BALB/c mice. However, their mechanisms of action were different because GIT-27NO released larger amounts of nitrite than Saq-NO in cell cultures and its antitumor action depended on the intracellular NO release inside the cells. On the contrary, Saq-NO released barely detectable amounts of NO and its antitumor action was NO-independent. In fact, cotreatment with an NO-peroxynitrite scavenger revealed that GIT-27NO but not Saq-NO acts through peroxynitrite-mediated cell destruction. At the cellular level, GIT-27NO prevalently induced proapoptotic signals followed by caspase-dependent apoptosis. In contrast, Saq-NO blocked cell proliferation, changed the adhesive, migratory, and invasive properties of the cells, and decreased metastatic potential in vivo. In conclusion, differences in NO release and oxidative stress generation between GIT-27NO and Saq-NO resulted in different mechanisms that caused cell death.en
dc.publisherAmer Soc Pharmacology Experimental Therapeutics, Bethesda
dc.relationinfo:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/173013/RS//
dc.rightsrestrictedAccess
dc.sourceMolecular Pharmacology
dc.titleTherapeutic Potential of Nitric Oxide-Modified Drugs in Colon Cancer Cellsen
dc.typearticle
dc.rights.licenseARR
dc.citation.epage710
dc.citation.issue4
dc.citation.other82(4): 700-710
dc.citation.rankM21
dc.citation.spage700
dc.citation.volume82
dc.identifier.doi10.1124/mol.112.077842
dc.identifier.pmid22798453
dc.identifier.scopus2-s2.0-84866853268
dc.identifier.wos000309509900015
dc.type.versionpublishedVersion


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