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dc.creatorLjujić, Mila
dc.creatorMijatović, Sanja
dc.creatorBulatović, Mirna Z.
dc.creatorMojic, Marija
dc.creatorMaksimović-Ivanić, Danijela
dc.creatorRadojković, Dragica
dc.creatorTopić, Aleksandra
dc.date.accessioned2019-09-02T11:56:49Z
dc.date.available2019-09-02T11:56:49Z
dc.date.issued2016
dc.identifier.issn0026-8933
dc.identifier.urihttp://farfar.pharmacy.bg.ac.rs/handle/123456789/2773
dc.description.abstractAlpha-1-antitrypsin (AAT), an acute phase protein, is the principal circulatory anti-protease. This multifunctional protein is encoded by the SERPINA1 gene. Although AAT was recognised as a potential tumour marker, its role in cancer biology remains unknown. Given that it has been demonstrated that AAT has an anti-apoptotic property against non-malignant cells, we aimed to investigate whether AAT affects apoptosis in a colon cancer cell line (HCT116). The presence of AAT in the HCT116 cell culture antagonized cytotoxicity of blockers of MEK1/2, PI3K/Akt pathways as well as NF-kappa B. The dominantly recovered cell viability was observed in the co-treatment with MEK1/2 inhibitor U0126. In addition, it was revealed that AAT almost completely abolished U0126-induced apoptosis through maintenance of the autophagy process. Our study revealed for the first time that the observed cyto-protection triggered by AAT was accompanied by sustained autophagy which opposed apoptosis. These results may contribute to understanding of the role of AAT in cancer development and evaluation of efficacy of cancer therapy.en
dc.publisherMaik Nauka/Interperiodica/Springer, New York
dc.relationinfo:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/173013/RS//
dc.rightsrestrictedAccess
dc.sourceMolecular Biology
dc.titleALPHA-1 Antitrypsin Affects U0126-Induced Cytotoxicity in Colon Cancer Cell Line (HCT116)en
dc.typearticle
dc.rights.licenseARR
dcterms.abstractБулатовић, Мирна З.; Мојиц, Марија; Топиц, Aлександра; Максимовић-Иванић, Данијела; Љујић, Мила; Радојковић, Драгица; Мијатовић, Сања;
dc.citation.volume50
dc.citation.issue1
dc.citation.spage153
dc.citation.epage156
dc.citation.other50(1): 153-156
dc.citation.rankM23
dc.identifier.wos000378140200018
dc.identifier.doi10.1134/S002689331601012X
dc.identifier.scopus2-s2.0-84961873039
dc.identifier.rcubconv_3601
dc.type.versionpublishedVersion


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