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Sökning: WFRF:(Gogvadze V)

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  • Abdrakhmanov, A, et al. (författare)
  • Receptor-Mediated Mitophagy Rescues Cancer Cells under Hypoxic Conditions
  • 2021
  • Ingår i: Cancers. - : MDPI AG. - 2072-6694. ; 13:16
  • Tidskriftsartikel (refereegranskat)abstract
    • Targeting mitochondria with thenoyltrifluoroacetone (TTFA), an inhibitor of Complex II in the respiratory chain, stimulated cisplatin-induced apoptosis in various cell lines in normoxia but not in hypoxia. This can be explained by the elimination of mitochondria involved in triggering apoptotic cell death by mitophagy, either Parkin-dependent or receptor-mediated. Treatment with TTFA alone or in combination with cisplatin did not cause accumulation of PINK1, meaning that under hypoxic conditions cells survive through activation of a receptor-mediated pathway. Hypoxia triggers the accumulation of BNIP3 and BNIP3L (also known as NIX), key participants in receptor-mediated mitophagy. Under hypoxic conditions, stimulation of autophagy, as assessed by the accumulation of lipidated form of LC3 (LC3II), was observed. To exclude the contribution of canonical macroautophagy in LC3II accumulation, experiments were performed using U1810 cells lacking ATG13, a key enzyme of macroautophagy. Despite the absence of ATG13, hypoxia-mediated accumulation of LC3II was not affected, underlying the importance of the receptor-mediated pathway. In order to prove the protective role of BNIP3 against cisplatin-induced apoptosis, BNIP3-deficient A549 cells were used. Surprisingly, a BNIP3 knockout did not abolish hypoxia-induced protection; however, in cells lacking BNIP3, a compensatory upregulation of BNIP3L was detected. Thus, in the absence of BNIP3, mitophagy could be maintained by BNIP3L and lead to cell death suppression due to the elimination of proapoptotic mitochondria. When both BNIP3 and BNIP3L were knocked out, the inhibitory effect of hypoxia on apoptosis was diminished, although not abolished completely. Undoubtedly, receptor-mediated mitophagy is likely to be one of the mechanisms responsible for cell death suppression under hypoxic conditions.
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  • Denisenko, TV, et al. (författare)
  • Mitophagy in carcinogenesis and cancer treatment
  • 2021
  • Ingår i: Discover. Oncology. - : Springer Science and Business Media LLC. - 2730-6011. ; 12:1, s. 58-
  • Tidskriftsartikel (refereegranskat)abstract
    • In order to maintain a functional mitochondrial network, cells have developed a quality control mechanism, namely mitophagy. This process can be induced through different pathways. The most studied is the so-called PINK1/Parkin pathway, which is associated with ubiquitylation of several mitochondrial proteins that were initially found to be related to Parkinson’s disease. Another type of mitophagy is known as receptor-mediated mitophagy, which includes proteins, such as BNIP3 and BNIP3L, also known as Nix. Through these two mechanisms, mitophagy fulfills its functions and maintains cellular homeostasis. Here, we summarize the current knowledge about the mechanisms of mitophagy regulation and their interplay with cancer progression as well as anticancer treatment.
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  • Gallud, A, et al. (författare)
  • Cationic gold nanoparticles elicit mitochondrial dysfunction: a multi-omics study
  • 2019
  • Ingår i: Scientific reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 9:1, s. 4366-
  • Tidskriftsartikel (refereegranskat)abstract
    • Systems biology is increasingly being applied in nanosafety research for observing and predicting the biological perturbations inflicted by exposure to nanoparticles (NPs). In the present study, we used a combined transcriptomics and proteomics approach to assess the responses of human monocytic cells to Au-NPs of two different sizes with three different surface functional groups, i.e., alkyl ammonium bromide, alkyl sodium carboxylate, or poly(ethylene glycol) (PEG)-terminated Au-NPs. Cytotoxicity screening using THP-1 cells revealed a pronounced cytotoxicity for the ammonium-terminated Au-NPs, while no cell death was seen after exposure to the carboxylated or PEG-modified Au-NPs. Moreover, Au-NR3+ NPs, but not the Au-COOH NPs, were found to trigger dose-dependent lethality in vivo in the model organism, Caenorhabditis elegans. RNA sequencing combined with mass spectrometry-based proteomics predicted that the ammonium-modified Au-NPs elicited mitochondrial dysfunction. The latter results were validated by using an array of assays to monitor mitochondrial function. Au-NR3+ NPs were localized in mitochondria of THP-1 cells. Moreover, the cationic Au-NPs triggered autophagy in macrophage-like RFP-GFP-LC3 reporter cells, and cell death was aggravated upon inhibition of autophagy. Taken together, these studies have disclosed mitochondria-dependent effects of cationic Au-NPs resulting in the rapid demise of the cells.
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  • Gladkovskaya, O, et al. (författare)
  • In one harness: the interplay of cellular responses and subsequent cell fate after quantum dot uptake
  • 2016
  • Ingår i: Nanomedicine (London, England). - : Future Medicine Ltd. - 1748-6963 .- 1743-5889. ; 11:19, s. 2603-2615
  • Tidskriftsartikel (refereegranskat)abstract
    • Rapid growth and expansion of engineered nanomaterials will occur when the technology can be used safely. Quantum dots have excellent prospects in clinical applications, but the issue of toxicity has not yet been resolved. To enable their medical implementation, the effect on, and mechanisms in, live cells should be clearly known and predicted. A massive amount of experimental data dedicated to nanotoxicity has been accumulated to-date, but it lacks a logical structure. The current challenge is to organize existing knowledge into lucid biological and mathematical models. In our review we aim to describe the interplay of various cell death mechanisms triggered by quantum dots as a consequence of particle parameters and experimental conditions.
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  • Glukhova, XA, et al. (författare)
  • Impairment of Fas-ligand-caveolin-1 interaction inhibits Fas-ligand translocation to rafts and Fas-ligand-induced cell death
  • 2018
  • Ingår i: Cell death & disease. - : Springer Science and Business Media LLC. - 2041-4889. ; 9:2, s. 73-
  • Tidskriftsartikel (refereegranskat)abstract
    • Fas-ligand/CD178 belongs to the TNF family proteins and can induce apoptosis through death receptor Fas/CD95. The important requirement for Fas-ligand-dependent cell death induction is its localization to rafts, cholesterol- and sphingolipid-enriched micro-domains of membrane, involved in regulation of different signaling complexes. Here, we demonstrate that Fas-ligand physically associates with caveolin-1, the main protein component of rafts. Experiments with cells overexpressing Fas-ligand revealed a FasL N-terminal pre-prolin-rich region, which is essential for the association with caveolin-1. We found that the N-terminal domain of Fas-ligand bears two caveolin-binding sites. The first caveolin-binding site binds the N-terminal domain of caveolin-1, whereas the second one appears to interact with the C-terminal domain of caveolin-1. The deletion of both caveolin-binding sites in Fas-ligand impairs its distribution between cellular membranes, and attenuates a Fas-ligand-induced cytotoxicity. These results demonstrate that the interaction of Fas-ligand and caveolin-1 represents a molecular basis for Fas-ligand translocation to rafts, and the subsequent induction of Fas-ligand-dependent cell death. A possibility of a similar association between other TNF family members and caveolin-1 is discussed.
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  • Gogvadze, V, et al. (författare)
  • Mitochondria--a bullseye in cancer therapy
  • 2014
  • Ingår i: Mitochondrion. - : Elsevier BV. - 1872-8278 .- 1567-7249. ; 1919 Pt A, s. 1-2
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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  • Gogvadze, V, et al. (författare)
  • Mitochondria as targets for chemotherapy
  • 2009
  • Ingår i: Apoptosis : an international journal on programmed cell death. - : Springer Science and Business Media LLC. - 1573-675X. ; 14:4, s. 624-640
  • Tidskriftsartikel (refereegranskat)
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  • Gogvadze, V (författare)
  • Targeting mitochondria in fighting cancer
  • 2011
  • Ingår i: Current pharmaceutical design. - : Bentham Science Publishers Ltd.. - 1873-4286 .- 1381-6128. ; 17:36, s. 4034-4046
  • Tidskriftsartikel (refereegranskat)
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  • Kulikov, AV, et al. (författare)
  • Cytochrome c: the Achilles' heel in apoptosis
  • 2012
  • Ingår i: Cellular and molecular life sciences : CMLS. - : Springer Science and Business Media LLC. - 1420-9071 .- 1420-682X. ; 69:11, s. 1787-1797
  • Tidskriftsartikel (refereegranskat)
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  • Resultat 1-50 av 88

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