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5-Aminoimidazole-4-carboxamide ribonucleoside-induced autophagy flux during differentiation of monocytic leukemia cells
Cell Death Discovery, 3 (2017); 17066. https://doi.org/10.1038/cddiscovery.2017.66
Dembitz, Vilma; Lalić, Hrvoje; Višnjić, Dora

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Dembitz, V., Lalić, H. i Višnjić, D. (2017). 5-Aminoimidazole-4-carboxamide ribonucleoside-induced autophagy flux during differentiation of monocytic leukemia cells. Cell Death Discovery, 3., 17066. doi: 10.1038/cddiscovery.2017.66

Dembitz, Vilma, et al. "5-Aminoimidazole-4-carboxamide ribonucleoside-induced autophagy flux during differentiation of monocytic leukemia cells." Cell Death Discovery, vol. 3, 2017, str. 17066. https://doi.org/10.1038/cddiscovery.2017.66

Dembitz, Vilma, Hrvoje Lalić i Dora Višnjić. "5-Aminoimidazole-4-carboxamide ribonucleoside-induced autophagy flux during differentiation of monocytic leukemia cells." Cell Death Discovery 3 (2017): 17066. https://doi.org/10.1038/cddiscovery.2017.66

Dembitz, V., Lalić, H. i Višnjić, D. (2017) '5-Aminoimidazole-4-carboxamide ribonucleoside-induced autophagy flux during differentiation of monocytic leukemia cells', Cell Death Discovery, 3, str. 17066. doi: 10.1038/cddiscovery.2017.66

Dembitz V, Lalić H, Višnjić D. 5-Aminoimidazole-4-carboxamide ribonucleoside-induced autophagy flux during differentiation of monocytic leukemia cells. Cell Death Discovery [Internet]. 02.10.2017. [pristupljeno 17.05.2024.];3:17066. doi: 10.1038/cddiscovery.2017.66

V. Dembitz, H. Lalić i D. Višnjić, "5-Aminoimidazole-4-carboxamide ribonucleoside-induced autophagy flux during differentiation of monocytic leukemia cells", Cell Death Discovery, vol. 3, str. 17066, Listopad 2017. [Online]. Dostupno na: https://urn.nsk.hr/urn:nbn:hr:105:431849. [Citirano: 17.05.2024.]

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Naslov (engleski)5-Aminoimidazole-4-carboxamide ribonucleoside-induced autophagy flux during differentiation of monocytic leukemia cells
AutorVilma Dembitz
AutorHrvoje Lalić
AutorDora Višnjić
Autorova ustanovaSveučilište u Zagrebu
Medicinski fakultet
Znanstveno / umjetničko
područje, polje i grana		BIOMEDICINA I ZDRAVSTVO
Kliničke medicinske znanosti
Sažetak (engleski)
Pharmacological modulators of AMP-dependent kinase (AMPK) have been suggested in treatment of cancer. The biguanide metformin and 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) have been reported to inhibit proliferation of solid tumors and hematological malignancies, but their role in differentiation is less explored. Our previous study demonstrated that AICAR alone induced AMPK-independent expression of differentiation markers in monocytic U937 leukemia cells, and no such effects were observed in response to metformin. The aim of this study was to determine the mechanism of AICAR-mediated effects and to test for the possible role of autophagy in differentiation of leukemia cells. The results showed that AICAR-mediated effects on the expression of differentiation markers were not mimicked by A769662, a more specific direct AMPK activator. Long-term incubation of U937 cells with AICAR and other differentiation agents, all-trans-retinoic acid (ATRA) and phorbol 12-myristate 13-acetate, increased the expression of the autophagy marker LC3B-II, and these effects were not observed in response to metformin. Western blot and immunofluorescence analyses of U937 cells treated with bafilomycin A1 or transfected with mRFP-GFP-LC3 proved that the increase in the expression of LC3B-II was due to an increase in autophagy flux, and not to a decrease in lysosomal degradation. 3-Methyladenine inhibited the expression of differentiation markers in response to all inducers, but had stimulatory effects on autophagy flux at dose that effectively inhibited the production of phosphatidylinositol 3-phosphate. The small inhibitory RNA-mediated down-modulation of Beclin 1 and hVPS34 had no effects on AICAR and ATRA-mediated increase in the expression of differentiation markers. These results show that AICAR and other differentiation agents induce autophagy flux in U937 cells and that the effects of AICAR and ATRA on the expression of differentiation markers do not depend on the normal levels of key proteins of the classical or canonical autophagy pathway.
Jezikengleski
Vrsta publikacijeZnanstveni rad - Izvorni znanstveni rad
Status objaveObjavljen
Vrsta recenzijeRecenziran
Verzija publikacijeObjavljena verzija rada (izdavačev PDF)
Naslov časopisaCell Death Discovery
Brojčani podacivol. 3, str. 17066
p-ISSN2058-7716
DOIhttps://doi.org/10.1038/cddiscovery.2017.66
URN:NBNurn:nbn:hr:105:431849
Datum objave publikacije2017-10-02
URL dokumentahttps://doi.org/10.1038/cddiscovery.2017.66
Vrsta resursaTekst
Prava pristupaOtvoreni pristup
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Datum i vrijeme pohrane2024-03-28 09:04:53