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  1. AU="Mishukov, Artem"
  2. AU="Ure, Benno M"
  3. AU="Mahmood, Mohammad Afzal"
  4. AU="Javaudin, François"
  5. AU="Morshed, K"
  6. AU="Portran, Philippe"
  7. AU="Xavier Coumoul"
  8. AU="Lutterer, S."
  9. AU="A Gasset-Teixidor"
  10. AU="Brea, Ángel"
  11. AU="Mozaherul Hoque Abdul Hasnat"
  12. AU="Adeyemi, Oluwapelumi O"
  13. AU="Oyim, James"
  14. AU="Fu, Yuntian"
  15. AU="Spigland, N"
  16. AU="Blum, Jonathan"
  17. AU="Philips, Santosh"
  18. AU="Lin, Xingyu"
  19. AU=Ko C W AU=Ko C W
  20. AU="Yang, Shucai"
  21. AU="Orton, Jane"
  22. AU="Remer, Thomas"
  23. AU="Blanco Álvarez, Adoración"
  24. AU="Nestor Laurier, Engone Obiang"
  25. AU="Huberty, Fanny"
  26. AU="Ju, Beomsoo"
  27. AU="Yu, Jessica"
  28. AU="Yamada, Hiroyuki"
  29. AU="Uruski, Pawel"
  30. AU="Laranjeiro, Ricardo"
  31. AU="Ahmadi, Reza"
  32. AU="Hoet, Peter H.M."
  33. AU=Sengupta Sohini AU=Sengupta Sohini
  34. AU="Conlon, Dara"
  35. AU=Endeman Henrik AU=Endeman Henrik
  36. AU="New, Sophie E.P"

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  1. Artikel ; Online: TR-57 Treatment of SUM159 Cells Induces Mitochondrial Dysfunction without Affecting Membrane Potential.

    Mishukov, Artem / Mndlyan, Ekaterina / Berezhnov, Alexey V / Kobyakova, Margarita / Lomovskaya, Yana / Holmuhamedov, Ekhson / Odinokova, Irina

    International journal of molecular sciences

    2024  Band 25, Heft 2

    Abstract: Recent works identified ClpXP, mitochondrial caseinolytic protease, as the only target of imipridones, a new class of antitumor agents. Our study of the mechanism of imipridone derivative TR-57 action in SUM159 human breast cancer cells demonstrated ... ...

    Abstract Recent works identified ClpXP, mitochondrial caseinolytic protease, as the only target of imipridones, a new class of antitumor agents. Our study of the mechanism of imipridone derivative TR-57 action in SUM159 human breast cancer cells demonstrated mitochondrial fragmentation, degradation of mitochondrial mtDNA and mitochondrial dysfunction due to inhibition of Complex I and Complex II activity. Complete inhibition of oxidative phosphorylation accompanied 90, 94, 88 and 87% decreases in the content of Complex I, II, III and IV proteins, respectively. The content of the F
    Mesh-Begriff(e) Humans ; Mitochondria ; Membrane Potential, Mitochondrial ; Adenosine Triphosphatases ; Adenine Nucleotide Translocator 2 ; Electron Transport Complex I ; Mitochondrial Diseases ; Adenosine Triphosphate
    Chemische Substanzen Adenosine Triphosphatases (EC 3.6.1.-) ; Adenine Nucleotide Translocator 2 ; Electron Transport Complex I (EC 7.1.1.2) ; Adenosine Triphosphate (8L70Q75FXE)
    Sprache Englisch
    Erscheinungsdatum 2024-01-18
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms25021193
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: Disulfiram oxy-derivatives induce entosis or paraptosis-like death in breast cancer MCF-7 cells depending on the duration of treatment

    Solovieva, Marina / Shatalin, Yuri / Odinokova, Irina / Krestinina, Olga / Baburina, Yulia / Mishukov, Artem / Lomovskaya, Yana / Pavlik, Liubov / Mikheeva, Irina / Holmuhamedov, Ekhson / Akatov, Vladimir

    Biochimica et biophysica acta. 2022 Sept., v. 1866, no. 9

    2022  

    Abstract: Dithiocarbamates and derivatives (including disulfiram, DSF) are currently investigated as antineoplastic agents. We have revealed earlier the ability of hydroxocobalamin (vitamin В₁₂b) combined with diethyldithiocarbamate (DDC) to catalyze the formation ...

    Abstract Dithiocarbamates and derivatives (including disulfiram, DSF) are currently investigated as antineoplastic agents. We have revealed earlier the ability of hydroxocobalamin (vitamin В₁₂b) combined with diethyldithiocarbamate (DDC) to catalyze the formation of highly cytotoxic oxidized derivatives of DSF (DSFoxy, sulfones and sulfoxides). Electron and fluorescent confocal microscopy, molecular biology and conventional biochemical techniques were used to study the morphological and functional responses of MCF-7 human breast cancer cells to treatment with DDC and B₁₂b alone or in combination. DDC induces unfolded protein response in MCF-7 cells. The combined use of DDC and B₁₂b causes MCF-7 cell death. Electron microscopy revealed the separation of ER and nuclear membranes, leading to the formation of both cytoplasmic and perinuclear vacuoles, with many fibers inside. The process of vacuolization coincided with the appearance of ER stress markers, a marked damage to mitochondria, a significant inhibition of 20S proteasome, and actin depolimerization at later stages. Specific inhibitors of apoptosis, necroptosis, autophagy, and ferroptosis did not prevent cell death. A short- time (6-h) exposure to DSFoxy caused a significant increase in the number of entotic cells. These observations indicate that MCF-7 cells treated with a mixture of DDC and B₁₂b die by the mechanism of paraptosis. A short- time exposure to DSFoxy caused, along with paraptosis, a significant activation of the entosis and its final stage, lysosomal cell death. The results obtained open up opportunities for the development of new approaches to induce non-apoptotic death of cancer cells by dithiocarbamates.
    Schlagwörter actin ; apoptosis ; autophagy ; breast neoplasms ; confocal microscopy ; cytotoxicity ; death ; disulfiram ; electron microscopy ; ferroptosis ; fluorescence ; human cell lines ; humans ; mitochondria ; molecular biology ; necroptosis ; oxidation ; proteasome endopeptidase complex ; sulfoxides ; unfolded protein response
    Sprache Englisch
    Erscheinungsverlauf 2022-09
    Erscheinungsort Elsevier B.V.
    Dokumenttyp Artikel
    ZDB-ID 840755-1
    ISSN 0304-4165
    ISSN 0304-4165
    DOI 10.1016/j.bbagen.2022.130184
    Datenquelle NAL Katalog (AGRICOLA)

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  3. Artikel ; Online: Disulfiram oxy-derivatives induce entosis or paraptosis-like death in breast cancer MCF-7 cells depending on the duration of treatment.

    Solovieva, Marina / Shatalin, Yuri / Odinokova, Irina / Krestinina, Olga / Baburina, Yulia / Mishukov, Artem / Lomovskaya, Yana / Pavlik, Liubov / Mikheeva, Irina / Holmuhamedov, Ekhson / Akatov, Vladimir

    Biochimica et biophysica acta. General subjects

    2022  Band 1866, Heft 9, Seite(n) 130184

    Abstract: Background: Dithiocarbamates and derivatives (including disulfiram, DSF) are currently investigated as antineoplastic agents. We have revealed earlier the ability of hydroxocobalamin (vitamin В: Methods: Electron and fluorescent confocal microscopy, ... ...

    Abstract Background: Dithiocarbamates and derivatives (including disulfiram, DSF) are currently investigated as antineoplastic agents. We have revealed earlier the ability of hydroxocobalamin (vitamin В
    Methods: Electron and fluorescent confocal microscopy, molecular biology and conventional biochemical techniques were used to study the morphological and functional responses of MCF-7 human breast cancer cells to treatment with DDC and B
    Results: DDC induces unfolded protein response in MCF-7 cells. The combined use of DDC and B
    Conclusions: These observations indicate that MCF-7 cells treated with a mixture of DDC and B
    General significance: The results obtained open up opportunities for the development of new approaches to induce non-apoptotic death of cancer cells by dithiocarbamates.
    Mesh-Begriff(e) Antineoplastic Agents/chemistry ; Antineoplastic Agents/pharmacology ; Breast Neoplasms/drug therapy ; Disulfiram/pharmacology ; Ditiocarb/chemistry ; Ditiocarb/pharmacology ; Duration of Therapy ; Entosis ; Female ; Humans ; MCF-7 Cells
    Chemische Substanzen Antineoplastic Agents ; Ditiocarb (99Z2744345) ; Disulfiram (TR3MLJ1UAI)
    Sprache Englisch
    Erscheinungsdatum 2022-06-01
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 60-7
    ISSN 1872-8006 ; 1879-2596 ; 1879-260X ; 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) 1872-8006 ; 1879-2596 ; 1879-260X ; 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.bbagen.2022.130184
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: ONC201-Induced Mitochondrial Dysfunction, Senescence-like Phenotype, and Sensitization of Cultured BT474 Human Breast Cancer Cells to TRAIL.

    Mishukov, Artem / Odinokova, Irina / Mndlyan, Ekaterina / Kobyakova, Margarita / Abdullaev, Serazhutdin / Zhalimov, Vitaly / Glukhova, Xenia / Galat, Vasiliy / Galat, Yekaterina / Senotov, Anatoly / Fadeev, Roman / Artykov, Artem / Gasparian, Marine E / Solovieva, Marina / Beletsky, Igor / Holmuhamedov, Ekhson

    International journal of molecular sciences

    2022  Band 23, Heft 24

    Abstract: ONC201, the anticancer drug, targets and activates mitochondrial ATP-dependent caseinolytic peptidase P (ClpP), a serine protease located in the mitochondrial matrix. Given the promise of ONC201 in cancer treatment, we evaluated its effects on the breast ...

    Abstract ONC201, the anticancer drug, targets and activates mitochondrial ATP-dependent caseinolytic peptidase P (ClpP), a serine protease located in the mitochondrial matrix. Given the promise of ONC201 in cancer treatment, we evaluated its effects on the breast ductal carcinoma cell line (BT474). We showed that the transient single-dose treatment of BT474 cells by 10 µM ONC201 for a period of less than 48 h induced a reversible growth arrest and a transient activation of an integrated stress response indicated by an increased expression of CHOP, ATF4, and GDF-15, and a reduced number of mtDNA nucleoids. A prolonged exposure to the drug (>48 h), however, initiated an irreversible loss of mtDNA, persistent activation of integrated stress response proteins, as well as cell cycle arrest, inhibition of proliferation, and suppression of the intrinsic apoptosis pathway. Since Natural Killer (NK) cells are quickly gaining momentum in cellular anti-cancer therapies, we evaluated the effect of ONC201 on the activity of the peripheral blood derived NK cells. We showed that following the ONC 201 exposure BT474 cells demonstrated enhanced sensitivity toward human NK cells that mediated killing. Together our data revealed that the effects of a single dose of ONC201 are dependent on the duration of exposure, specifically, while short-term exposure led to reversible changes; long-term exposure resulted in irreversible transformation of cells associated with the senescent phenotype. Our data further demonstrated that when used in combination with NK cells, ONC201 created a synergistic anti-cancer effect, thus suggesting its possible benefit in NK-cell based cellular immunotherapies for cancer treatment.
    Mesh-Begriff(e) Humans ; Female ; Breast Neoplasms/drug therapy ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Cell Line, Tumor ; Mitochondria ; DNA, Mitochondrial
    Chemische Substanzen TIC10 compound (9U35A31JAI) ; Antineoplastic Agents ; DNA, Mitochondrial
    Sprache Englisch
    Erscheinungsdatum 2022-12-08
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms232415551
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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