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MAP kinase-dependent autophagy controls phorbol myristate acetate-induced macrophage differentiation of HL-60 leukemia cells.

2022
Аутори:
Mandić, Miloš
Misirkić Marjanović, Maja
Vučićević, Ljubica
Jovanović, Maja
Bošnjak, Mihajlo
Perović, Vladimir
Ristić, Biljana
Ćirić, Darko
Harhaji Trajković, Ljubica
Trajković, Vladimir
Тип документа:
Чланак у часопису (Објављена верзија)
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© 2022 Elsevier Inc.
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Апстракт:
We investigated the mechanisms and the role of autophagy in the differentiation of HL-60 human acute myeloid leukemia cells induced by protein kinase C (PKC) activator phorbol myristate acetate (PMA). PMA-triggered differentiation of HL-60 cells into macrophage-like cells was confirmed by cell-cycle arrest accompanied by elevated expression of macrophage markers CD11b, CD13, CD14, CD45, EGR1, CSF1R, and IL-8. The induction of autophagy was demonstrated by the increase in intracellular acidification, accumulation/punctuation of autophagosome marker LC3-II, and the increase in autophagic flux. PMA also increased nuclear translocation of autophagy transcription factors TFEB, FOXO1, and FOXO3, as well as the expression of several autophagy-related (ATG) genes in HL-60 cells. PMA failed to activate autophagy inducer AMP-activated protein kinase (AMPK) and inhibit autophagy suppressor mechanistic target of rapamycin complex 1 (mTORC1). On the other hand, it readily stimulated the phosphorylation of mitogen-activated protein (MAP) kinases extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) via a protein kinase C-dependent mechanism. Pharmacological or genetic inhibition of ERK or JNK suppressed PMA-triggered nuclear translocation of TFEB and FOXO1/3, ATG expression, dissociation of pro-autophagic beclin-1 from its inhibitor BCL2, autophagy induction, and differentiation of HL-60 cells into macrophage-like cells. Pharmacological or genetic inhibition of autophagy also blocked PMA-induced macrophage differentiation of HL-60 cells. Therefore, MAP kinases ERK and JNK control PMA-induced macrophage differentiation of HL-60 leukemia cells through AMPK/mTORC1-independent, TFEB/FOXO-mediated transcriptional and beclin-1-dependent post-translational activation of autophagy.
Кључне речи:
Autophagy; Beclin-1; Differentiation; ERK; JNK; Leukemia
Извор:
Life Sciences, 2022, 297, 120481-
Финансирање / пројекти:
  • Министарство просвете, науке и технолошког развоја Републике Србије, Уговор бр. 200007 (Универзитет у Београду, Институт за биолошка истраживања 'Синиша Станковић') (RS-200007)
  • Министарство просвете, науке и технолошког развоја Републике Србије, Уговор бр. 200110 (Универзитет у Београду, Медицински факултет) (RS-200110)
  • COST Action CA15138

DOI: 10.1016/j.lfs.2022.120481

ISSN: 0024-3205

PubMed: 35304128

WoS: 000793214700005

Scopus: 2-s2.0-85126891813
[ Google Scholar ]
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URI
https://linkinghub.elsevier.com/retrieve/pii/S0024320522001813
http://www.ncbi.nlm.nih.gov/pubmed/35304128
http://radar.ibiss.bg.ac.rs/handle/123456789/4947
Колекције
  • Article
  • Article
Институција/група
IBISS
APA:
Mandic, M., Misirkic Marjanovic, M., Vucicevic, L., Jovanovic, M., Bosnjak, M., Perovic, V., et al. (2022). MAP kinase-dependent autophagy controls phorbol myristate acetate-induced macrophage differentiation of HL-60 leukemia cells. Life Sciences, 297, 120481.
Vancouver:
Mandic M, Misirkic Marjanovic M, Vucicevic L, Jovanovic M, Bosnjak M, Perovic V, Ristic B, Ciric D, Harhaji-Trajkovic L, Trajkovic V. MAP kinase-dependent autophagy controls phorbol myristate acetate-induced macrophage differentiation of HL-60 leukemia cells. Life Sci. 2022;297:120481.

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