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  1. AU="Konjeti R. Sekhar"
  2. AU="Dufresne, Eric M"
  3. AU="Pérez-Monje, Dan A"
  4. AU="Gazzola, Stefania"
  5. AU="Gruner, William"
  6. AU="Didichenko, Svetlana A"
  7. AU="Milone F."
  8. AU="Bianski, Brandon"
  9. AU="Swan, Aili"
  10. AU="Cao, Mengli"
  11. AU="Rayya, W."
  12. AU="Bleher, Jana"
  13. AU="Fong, Fuk-Kei"
  14. AU="Bouvier, Nicolas"
  15. AU="Mims, Catherine"
  16. AU="Abbasi, Ardeshir"
  17. AU="Gailey, Samantha" AU="Gailey, Samantha"
  18. AU="Yano, Shuya"
  19. AU="Balaur, Eugeniu"
  20. AU="Ağaçfidan, Ali"
  21. AU="Perkins, James A."
  22. AU="Arkoun, Brahim"

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  1. Artikel ; Online: Glutathione peroxidase 4 inhibition induces ferroptosis and mTOR pathway suppression in thyroid cancer

    Konjeti R. Sekhar / David N. Hanna / Sriram Cyr / Jordan J. Baechle / Sudhakiranmayi Kuravi / Ramesh Balusu / Kimryn Rathmell / Naira Baregamian

    Scientific Reports, Vol 12, Iss 1, Pp 1-

    2022  Band 10

    Abstract: Abstract Papillary thyroid carcinoma (PTC) demonstrates significantly reduced patient survival with metastatic progression. Tumor progression can be influenced by metabolism, including antioxidant glutathione (GSH). Glutathione peroxidase 4 (GPX4) is a ... ...

    Abstract Abstract Papillary thyroid carcinoma (PTC) demonstrates significantly reduced patient survival with metastatic progression. Tumor progression can be influenced by metabolism, including antioxidant glutathione (GSH). Glutathione peroxidase 4 (GPX4) is a selenoenzyme that uses GSH as a co-factor to regulate lipid peroxidation of cell membranes during increased oxidative stress. GPX4 suppression in tumor cells can induce ferroptosis. This study aims to examine ferroptosis as a potentially critical pathway in effective targeting of thyroid cancer (TC) cells. We treated human TC cells (K1, MDA-T68, MDA-T32, TPC1) with (1S,3R)-RSL3 (RSL3), a small-molecule inhibitor of GPX4 and examined the effects on ferroptosis, tumor cell survival and migration, spheroid formation, oxidative stress, DNA damage repair response, and mTOR signaling pathway in vitro. GPX4 inhibition activated ferroptosis, inducing TC cell death, rapid rise in reactive oxygen species and effectively arrested cell migration in vitro. Suppression of mTOR signaling pathway triggered autophagy. GPX4 genetic knockdown mirrored RSL3 effect on mTOR pathway suppression. RSL3 subdued DNA damage repair response by suppressing phosphorylation of nucleophosmin 1 (NPM1). Thus, observed potent induction of ferroptosis, GPX4-dependent novel suppression of mTOR pathway and DNA damage repair response in preclinical in vitro model of TC supports GPX4 targeting for therapeutic benefit in advanced therapy-resistant thyroid cancers.
    Schlagwörter Medicine ; R ; Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2022-11-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: Radiosensitization by enzalutamide for human prostate cancer is mediated through the DNA damage repair pathway.

    Konjeti R Sekhar / Jian Wang / Michael L Freeman / Austin N Kirschner

    PLoS ONE, Vol 14, Iss 4, p e

    2019  Band 0214670

    Abstract: Radiation therapy is often combined with androgen deprivation therapy in the treatment of aggressive localized prostate cancer. However, castration-resistant disease may not respond to testosterone deprivation approaches. Enzalutamide is a second- ... ...

    Abstract Radiation therapy is often combined with androgen deprivation therapy in the treatment of aggressive localized prostate cancer. However, castration-resistant disease may not respond to testosterone deprivation approaches. Enzalutamide is a second-generation anti-androgen with high affinity and activity that is used for the treatment of metastatic disease. Although radiosensitization mechanisms are known to be mediated through androgen receptor activity, this project aims to uncover the detailed DNA damage repair factors influenced by enzalutamide using multiple models of androgen-sensitive (LNCaP) and castration-resistant human prostate cancer (22Rv1 and DU145). Enzalutamide is able to radiosensitize both androgen-dependent and androgen-independent human prostate cancer models in cell culture and xenografts in mice, as well as a treatment-resistant patient-derived xenograft. The enzalutamide-mediated mechanism of radiosensitization includes delay of DNA repair through temporal prolongation of the repair factor complexes and halting the cell cycle, which results in decreased colony survival. Altogether, these findings support the use of enzalutamide concurrently with radiotherapy to enhance the treatment efficacy for prostate cancer.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2019-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

    Volltext online

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    Kategorien

    Fernleihe an ZB MED

    Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

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