The antiproliferative effects of chicken anemia virus-derived protein apoptin toward cancer stem cells (CROSBI ID 617861)
Prilog sa skupa u zborniku | sažetak izlaganja sa skupa | domaća recenzija
Podaci o odgovornosti
Ester Katja ; Jurlin Jelena ; Mikecin Ana-Matea ; Kralj Marijeta
engleski
The antiproliferative effects of chicken anemia virus-derived protein apoptin toward cancer stem cells
Apoptin, a protein from chicken anemia virus, has the ability to kill human tumor cells. It accumulates in the cytoplasm of normal cells, where it will be subsequently degraded by proteasomal activity. In tumor cells, apoptin enters the nucleus and redirects cell signaling toward apoptosis. It has been found that apoptin senses early stages of malignant transformation, but it is not clear what follows these early changes in cells that would be recognized by the apoptin. In the study presented here, antiproliferative activities of apoptin toward cancer stem cells were compared to its effects toward other tumor cell lines. Transformed primary mammary epithelial cells (HMLE) with silenced gene for E cadherin (HMLE- shEcad) were used as a cancer stem cells (CSC) model. These cells were experimentally induced to pass through epithelial-mesenchymal transition, what was sufficient to acquire stem cells properties. An adenoviral vector that expresses Flag-tagged apoptin gene and a control vector that expresses lacZ gene were used to transfect cells. Localization within the cells, antiproliferative activity, different modes of programmed cell death, and cell cycle disturbances upon Ad-Ap infection were investigated. Although efficiency of transduction was low in the HMLE-shEcad cells, modest growth inhibition was measured. Apoptin localised in the nucleus of HMLE-shEcad cells, but it was not sufficient to induce apoptosis. Apoptin induced cell cycle G2 arrest 24 hours after infection, which delayed cell’s growth, but cells overcame this effect and recovered later. Apoptin showed distinct levels of cytotoxicity towards various tumor cell lines, identifying NCI-H1299 (non-small cell lung cancer) as the most sensitive. In these cells apoptin induced apoptosis, and also modulated autophagy. Our study confirmed apoptin as a potent tumor-cell killer, able to modulate different modes of programmed cell’s death, and moreover, to interfere with CSC. Mechanisms of CSC resistance to apoptin should be further analyzed and evaluated in more details.
apoptin; cell cycle; apoptosis; cancer stem cells
nije evidentirano
nije evidentirano
nije evidentirano
nije evidentirano
nije evidentirano
nije evidentirano
Podaci o prilogu
20-21.
2014.
objavljeno
Podaci o matičnoj publikaciji
1st Croviwo Croatian Virus Workshop, Basic and Translational Virus Research Book of Abstract
Vanda Juranić Lisnić, Igor Jurak and Dijana Škorić
Zagreb: Hrvatsko mikrobiološko društvo
978-953-7778-09-5
Podaci o skupu
1st CroViWo - Croatian Virus Workshop - Basic and Translational Virus Research
poster
14.11.2014-14.11.2014
Rijeka, Hrvatska