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Article: The Exploitation of Lysosomes in Cancer Therapy with Graphene-Based Nanomaterials.

Ristic, Biljana / Bosnjak, Mihajlo / Misirkic Marjanovic, Maja / Stevanovic, Danijela / Janjetovic, Kristina / Harhaji-Trajkovic, Ljubica

Pharmaceutics

2023 Volume 15, Issue 7

Abstract: Graphene-based nanomaterials (GNMs), including graphene, graphene oxide, reduced graphene oxide, and graphene quantum dots, may have direct anticancer activity or be used as nanocarriers for antitumor drugs. GNMs usually enter tumor cells by endocytosis ... ...

Abstract	Graphene-based nanomaterials (GNMs), including graphene, graphene oxide, reduced graphene oxide, and graphene quantum dots, may have direct anticancer activity or be used as nanocarriers for antitumor drugs. GNMs usually enter tumor cells by endocytosis and can accumulate in lysosomes. This accumulation prevents drugs bound to GNMs from reaching their targets, suppressing their anticancer effects. A number of chemical modifications are made to GNMs to facilitate the separation of anticancer drugs from GNMs at low lysosomal pH and to enable the lysosomal escape of drugs. Lysosomal escape may be associated with oxidative stress, permeabilization of the unstable membrane of cancer cell lysosomes, release of lysosomal enzymes into the cytoplasm, and cell death. GNMs can prevent or stimulate tumor cell death by inducing protective autophagy or suppressing autolysosomal degradation, respectively. Furthermore, because GNMs prevent bound fluorescent agents from emitting light, their separation in lysosomes may enable tumor cell identification and therapy monitoring. In this review, we explain how the characteristics of the lysosomal microenvironment and the unique features of tumor cell lysosomes can be exploited for GNM-based cancer therapy.
Language	English
Publishing date	2023-06-28
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527217-2
ISSN	1999-4923
ISSN	1999-4923
DOI	10.3390/pharmaceutics15071846
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Article: Modulation of Cancer Cell Autophagic Responses by Graphene-Based Nanomaterials: Molecular Mechanisms and Therapeutic Implications.

Ristic, Biljana / Harhaji-Trajkovic, Ljubica / Bosnjak, Mihajlo / Dakic, Ivana / Mijatovic, Srdjan / Trajkovic, Vladimir

Cancers

2021 Volume 13, Issue 16

Abstract: Graphene-based nanomaterials (GNM) are plausible candidates for cancer therapeutics and drug delivery systems. Pure graphene and graphene oxide nanoparticles, as well as graphene quantum dots and graphene nanofibers, were all able to trigger autophagy in ...

Abstract	Graphene-based nanomaterials (GNM) are plausible candidates for cancer therapeutics and drug delivery systems. Pure graphene and graphene oxide nanoparticles, as well as graphene quantum dots and graphene nanofibers, were all able to trigger autophagy in cancer cells through both transcriptional and post-transcriptional mechanisms involving oxidative/endoplasmic reticulum stress, AMP-activated protein kinase, mechanistic target of rapamycin, mitogen-activated protein kinase, and Toll-like receptor signaling. This was often coupled with lysosomal dysfunction and subsequent blockade of autophagic flux, which additionally increased the accumulation of autophagy mediators that participated in apoptotic, necrotic, or necroptotic death of cancer cells and influenced the immune response against the tumor. In this review, we analyze molecular mechanisms and structure-activity relationships of GNM-mediated autophagy modulation, its consequences for cancer cell survival/death and anti-tumor immune response, and the possible implications for the use of GNM in cancer therapy.
Language	English
Publishing date	2021-08-18
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13164145
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Article ; Online: Combination of Ascorbic Acid and Menadione Induces Cytotoxic Autophagy in Human Glioblastoma Cells.

Despotović, Ana / Mirčić, Aleksandar / Misirlić-Denčić, Sonja / Harhaji-Trajković, Ljubica / Trajković, Vladimir / Zogović, Nevena / Tovilović-Kovačević, Gordana

Oxidative medicine and cellular longevity

2022 Volume 2022, Page(s) 2998132

Abstract: We investigated the ability of the ascorbic acid (AA) and menadione (MD) combination, the well-known reactive oxidative species- (ROS-) generating system, to induce autophagy in human U251 glioblastoma cells. A combination of AA and MD (AA+MD), in ... ...

Abstract	We investigated the ability of the ascorbic acid (AA) and menadione (MD) combination, the well-known reactive oxidative species- (ROS-) generating system, to induce autophagy in human U251 glioblastoma cells. A combination of AA and MD (AA+MD), in contrast to single treatments, induced necrosis-like cell death mediated by mitochondrial membrane depolarization and extremely high oxidative stress. AA+MD, and to a lesser extent MD alone, prompted the appearance of autophagy markers such as autophagic vacuoles, autophagosome-associated LC3-II protein, degradation of p62, and increased expression of beclin-1. While both MD and AA+MD increased phosphorylation of AMP-activated protein kinase (AMPK), the well-known autophagy promotor, only the combined treatment affected its downstream targets, mechanistic target of rapamycin complex 1 (mTORC1), Unc 51-like kinase 1 (ULK1), and increased the expression of several autophagy-related genes. Antioxidant N-acetyl cysteine reduced both MD- and AA+MD-induced autophagy, as well as changes in AMPK/mTORC1/ULK1 activity and cell death triggered by the drug combination. Pharmacological and genetic autophagy silencing abolished the toxicity of AA+MD, while autophagy upregulation enhanced the toxicity of both AA+MD and MD. Therefore, by upregulating oxidative stress, inhibiting mTORC1, and activating ULK1, AA converts MD-induced AMPK-dependent autophagy from nontoxic to cytotoxic. These results suggest that AA+MD or MD treatment in combination with autophagy inducers could be further investigated as a novel approach for glioblastoma therapy.
MeSH term(s)	Ascorbic Acid/pharmacology ; Autophagy/physiology ; Glioblastoma/drug therapy ; Humans ; TOR Serine-Threonine Kinases/metabolism ; Vitamin K 3/pharmacology
Chemical Substances	Vitamin K 3 (723JX6CXY5) ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Ascorbic Acid (PQ6CK8PD0R)
Language	English
Publishing date	2022-03-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	2455981-7
ISSN	1942-0994 ; 1942-0994
ISSN (online)	1942-0994
ISSN	1942-0994
DOI	10.1155/2022/2998132
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Article: MAP kinase-dependent autophagy controls phorbol myristate acetate-induced macrophage differentiation of HL-60 leukemia cells

Mandic, Milos / Misirkic Marjanovic, Maja / Vucicevic, Ljubica / Jovanovic, Maja / Bosnjak, Mihajlo / Perovic, Vladimir / Ristic, Biljana / Ciric, Darko / Harhaji-Trajkovic, Ljubica / Trajkovic, Vladimir

Life sciences. 2022 May 15, v. 297

2022

Abstract: 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 ... ...

Abstract	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.
Keywords	AMP-activated protein kinase ; acetates ; acidification ; autophagosomes ; autophagy ; cell cycle checkpoints ; dissociation ; humans ; interleukin-8 ; macrophages ; mitogen-activated protein kinase ; myeloid leukemia ; phosphorylation ; protein kinase C ; rapamycin ; transcription (genetics)
Language	English
Dates of publication	2022-0515
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2022.120481
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Article ; Online: Dual targeting of tumor cell energy metabolism and lysosomes as an anticancer strategy.

Paunovic, Verica / Kosic, Milica / Misirkic-Marjanovic, Maja / Trajkovic, Vladimir / Harhaji-Trajkovic, Ljubica

Biochimica et biophysica acta. Molecular cell research

2020 Volume 1868, Issue 4, Page(s) 118944

Abstract: To sustain their proliferative and metastatic capacity, tumor cells increase the activity of energy-producing pathways and lysosomal compartment, resorting to autophagolysosomal degradation when nutrients are scarce. Consequently, large fragile lysosomes ...

Abstract	To sustain their proliferative and metastatic capacity, tumor cells increase the activity of energy-producing pathways and lysosomal compartment, resorting to autophagolysosomal degradation when nutrients are scarce. Consequently, large fragile lysosomes and enhanced energy metabolism may serve as targets for anticancer therapy. A simultaneous induction of energy stress (by caloric restriction and inhibition of glycolysis, oxidative phosphorylation, Krebs cycle, or amino acid/fatty acid metabolism) and lysosomal stress (by lysosomotropic detergents, vacuolar ATPase inhibitors, or cationic amphiphilic drugs) is an efficient anti-cancer strategy demonstrated in a number of studies. However, the mechanisms of lysosomal/energy stress co-amplification, apart from the protective autophagy inhibition, are poorly understood. We here summarize the established and suggest potential mechanisms and candidates for anticancer therapy based on the dual targeting of lysosomes and energy metabolism.
MeSH term(s)	Antineoplastic Combined Chemotherapy Protocols/pharmacology ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Autophagy ; Energy Metabolism/drug effects ; Humans ; Lysosomes/drug effects ; Lysosomes/metabolism ; Neoplasms/drug therapy ; Neoplasms/metabolism
Language	English
Publishing date	2020-12-28
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbamcr.2020.118944
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Article ; Online: Autophagy Receptor p62 Regulates SARS-CoV-2-Induced Inflammation in COVID-19.

Paunovic, Verica / Vucicevic, Ljubica / Misirkic Marjanovic, Maja / Perovic, Vladimir / Ristic, Biljana / Bosnjak, Mihajlo / Mandic, Milos / Stevanovic, Danijela / Harhaji-Trajkovic, Ljubica / Lalosevic, Jovan / Nikolic, Milos / Bonaci-Nikolic, Branka / Trajkovic, Vladimir

Cells

2023 Volume 12, Issue 9

Abstract: As autophagy can promote or inhibit inflammation, we examined autophagy-inflammation interplay in COVID-19. Autophagy markers in the blood of 19 control subjects and 26 COVID-19 patients at hospital admission and one week later were measured by ELISA, ... ...

Abstract	As autophagy can promote or inhibit inflammation, we examined autophagy-inflammation interplay in COVID-19. Autophagy markers in the blood of 19 control subjects and 26 COVID-19 patients at hospital admission and one week later were measured by ELISA, while cytokine levels were examined by flow cytometric bead immunoassay. The antiviral IFN-α and proinflammatory TNF, IL-6, IL-8, IL-17, IL-33, and IFN-γ were elevated in COVID-19 patients at both time points, while IL-10 and IL-1β were increased at admission and one week later, respectively. Autophagy markers LC3 and ATG5 were unaltered in COVID-19. In contrast, the concentration of autophagic cargo receptor p62 was significantly lower and positively correlated with TNF, IL-10, IL-17, and IL-33 at hospital admission, returning to normal levels after one week. The expression of SARS-CoV-2 proteins NSP5 or ORF3a in THP-1 monocytes caused an autophagy-independent decrease or autophagy-inhibition-dependent increase, respectively, of intracellular/secreted p62, as confirmed by immunoblot/ELISA. This was associated with an NSP5-mediated decrease in TNF/IL-10 mRNA and an ORF3a-mediated increase in TNF/IL-1β/IL-6/IL-10/IL-33 mRNA levels. A genetic knockdown of p62 mimicked the immunosuppressive effect of NSP5, and a p62 increase in autophagy-deficient cells mirrored the immunostimulatory action of ORF3a. In conclusion, the proinflammatory autophagy receptor p62 is reduced inacute COVID-19, and the balance between autophagy-independent decrease and autophagy blockade-dependent increase of p62 levels could affect SARS-CoV-induced inflammation.
MeSH term(s)	Humans ; Autophagy ; COVID-19/pathology ; Inflammation/metabolism ; Interleukin-10/blood ; Interleukin-17/blood ; Interleukin-33/blood ; Interleukin-6/blood ; RNA, Messenger ; SARS-CoV-2
Chemical Substances	Interleukin-10 (130068-27-8) ; Interleukin-17 ; Interleukin-33 ; Interleukin-6 ; RNA, Messenger ; nuclear pore protein p62
Language	English
Publishing date	2023-04-28
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12091282
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Article ; Online: 3-Methyladenine prevents energy stress-induced necrotic death of melanoma cells through autophagy-independent mechanisms.

Kosic, Milica / Paunovic, Verica / Ristic, Biljana / Mircic, Aleksandar / Bosnjak, Mihajlo / Stevanovic, Danijela / Kravic-Stevovic, Tamara / Trajkovic, Vladimir / Harhaji-Trajkovic, Ljubica

Journal of pharmacological sciences

2021 Volume 147, Issue 1, Page(s) 156–167

Abstract: We investigated the effect of 3-methyladenine (3MA), a class III phosphatidylinositol 3-kinase (PI3K)-blocking autophagy inhibitor, on cancer cell death induced by simultaneous inhibition of glycolysis by 2-deoxyglucose (2DG) and mitochondrial ... ...

Abstract	We investigated the effect of 3-methyladenine (3MA), a class III phosphatidylinositol 3-kinase (PI3K)-blocking autophagy inhibitor, on cancer cell death induced by simultaneous inhibition of glycolysis by 2-deoxyglucose (2DG) and mitochondrial respiration by rotenone. 2DG/rotenone reduced ATP levels and increased mitochondrial superoxide production, causing mitochondrial swelling and necrotic death in various cancer cell lines. 2DG/rotenone failed to increase proautophagic beclin-1 and autophagic flux in melanoma cells despite the activation of AMP-activated protein kinase (AMPK) and inhibition of mechanistic target of rapamycin complex 1 (mTORC1). 3MA, but not autophagy inhibition with other PI3K and lysosomal inhibitors, attenuated 2DG/rotenone-induced mitochondrial damage, oxidative stress, ATP depletion, and cell death, while antioxidant treatment mimicked its protective action. The protection was not mediated by autophagy upregulation via class I PI3K/Akt inhibition, as it was preserved in cells with genetically inhibited autophagy. 3MA increased AMPK and mTORC1 activation in energy-stressed cells, but neither AMPK nor mTORC1 inhibition reduced its cytoprotective effect. 3MA reduced JNK activation, and JNK pharmacological/genetic suppression mimicked its mitochondria-preserving and cytoprotective activity. Therefore, 3MA prevents energy stress-triggered cancer cell death through autophagy-independent mechanisms possibly involving JNK suppression and decrease of oxidative stress. Our results warrant caution when using 3MA as an autophagy inhibitor.
MeSH term(s)	AMP-Activated Protein Kinases/metabolism ; Adenine/analogs & derivatives ; Adenine/pharmacology ; Animals ; Autophagy/drug effects ; Cell Death/drug effects ; Deoxyglucose/pharmacology ; JNK Mitogen-Activated Protein Kinases/metabolism ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Melanoma/metabolism ; Melanoma/pathology ; Melanoma, Experimental ; Mice, Inbred C57BL ; Mitochondria/metabolism ; Mitochondrial Swelling ; Necrosis ; Oxidative Stress/drug effects ; Phosphatidylinositol 3-Kinases/metabolism ; Rotenone/pharmacology ; Mice
Chemical Substances	Rotenone (03L9OT429T) ; 3-methyladenine (5142-23-4) ; Deoxyglucose (9G2MP84A8W) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Adenine (JAC85A2161)
Language	English
Publishing date	2021-06-11
Publishing country	Japan
Document type	Journal Article
ZDB-ID	2104264-0
ISSN	1347-8648 ; 1347-8613
ISSN (online)	1347-8648
ISSN	1347-8613
DOI	10.1016/j.jphs.2021.06.003
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Article ; Online: MAP kinase-dependent autophagy controls phorbol myristate acetate-induced macrophage differentiation of HL-60 leukemia cells.

Life sciences

2022 Volume 297, Page(s) 120481

Abstract	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.
MeSH term(s)	Autophagy ; Extracellular Signal-Regulated MAP Kinases/metabolism ; HL-60 Cells ; Humans ; Leukemia ; Macrophages/metabolism ; Tetradecanoylphorbol Acetate/metabolism ; Tetradecanoylphorbol Acetate/pharmacology
Chemical Substances	Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; Tetradecanoylphorbol Acetate (NI40JAQ945)
Language	English
Publishing date	2022-03-15
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2022.120481
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Article ; Online: Mechanisms and therapeutic significance of autophagy modulation by antipsychotic drugs.

Vucicevic, Ljubica / Misirkic-Marjanovic, Maja / Harhaji-Trajkovic, Ljubica / Maric, Nadja / Trajkovic, Vladimir

Cell stress

2018 Volume 2, Issue 11, Page(s) 282–291

Abstract: In this review we analyze the ability of antipsychotic medications to modulate macroautophagy, a process of controlled lysosomal digestion of cellular macromolecules and organelles. We focus on its molecular mechanisms, consequences for the function/ ... ...

Abstract	In this review we analyze the ability of antipsychotic medications to modulate macroautophagy, a process of controlled lysosomal digestion of cellular macromolecules and organelles. We focus on its molecular mechanisms, consequences for the function/survival of neuronal and other cells, and the contribution to the beneficial and side-effects of antipsychotics in the treatment of schizophrenia, neurodegeneration, and cancer. A wide range of antipsychotics was able to induce neuronal autophagy as a part of the adaptive stress response apparently independent of mammalian target of rapamycin and dopamine receptor blockade. Autophagy induction by antipsychotics could contribute to reducing neuronal dysfunction in schizophrenia, but also to the adverse effects associated with their long-term use, such as brain volume loss and weight gain. In neurodegenerative diseases, antipsychotic-stimulated autophagy might help to increase the clearance and reduce neurotoxicity of aggregated proteotoxins. However, the possibility that some antipsychotics might block autophagic flux and potentially contribute to proteotoxin-mediated neurodegeneration must be considered. Finally, the anticancer effects of autophagy induction by antipsychotics make plausible their repurposing as adjuncts to standard cancer therapy.
Language	English
Publishing date	2018-10-25
Publishing country	Austria
Document type	Journal Article ; Review
ISSN	2523-0204
ISSN (online)	2523-0204
DOI	10.15698/cst2018.11.161
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Article: Data supporting the inability of indomethacin to induce autophagy in U251 glioma cells

Pantovic, Aleksandar / Arsikin, Katarina / Kosic, Milica / Ristic, Biljana / Trajkovic, Vladimir / Harhaji-Trajkovic, Ljubica

Data in Brief. 2017 Apr., v. 11

2017

Abstract: Autophagy, a catabolic process involving intracellular degradation of unnecessary or dysfunctional cellular components through the lysosomal machinery, could act as a prosurvival, as well as a cytotoxic mechanism (Parzych and Klionsky, 2014) [1]. ... ...

Abstract	Autophagy, a catabolic process involving intracellular degradation of unnecessary or dysfunctional cellular components through the lysosomal machinery, could act as a prosurvival, as well as a cytotoxic mechanism (Parzych and Klionsky, 2014) [1]. Cyclooxygenase inhibitor indomethacin inhibits proliferation of glioma cells, and has been reported to reduce the activity of the main autophagy repressor mammalian target of rapamycin (mTOR) (Pantovic et al., 2016) [2]. Here we investigated the ability of indomethacin to induce autophagy in U251 human glioma cells. We assessed the influence of indomethacin on intracellular acidification, expression of proautophagic protein beclin-1, and conversion of microtubule-associated protein light chain 3-I (LC3-I) to autophagosome-associated LC3-II, in the presence or absence of lysosomal inhibitors. The effect of genetic and pharmacological downregulation of autophagy on the cytotoxicity of indomethacin was also evaluated. The interpretation of these data can be found in “In vitro antiglioma action of indomethacin is mediated via AMP-activated protein kinase/mTOR complex 1 signaling pathway” (Pantovic et al., 2016; doi:10.1016/j.biocel.2016.12.007) [2].
Keywords	AMP-activated protein kinase ; acidification ; autophagy ; catabolism ; cyclooxygenase inhibitors ; cytotoxicity ; glioma ; humans ; indomethacin ; rapamycin
Language	English
Dates of publication	2017-04
Size	p. 225-230.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	2786545-9
ISSN	2352-3409
ISSN	2352-3409
DOI	10.1016/j.dib.2017.02.012
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