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Author De Backer, J.; Maric, D.; Zuhra, K.; Bogaerts, A.; Szabo, C.; Vanden Berghe, W.; Hoogewijs, D. url  doi
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  Title Cytoglobin Silencing Promotes Melanoma Malignancy but Sensitizes for Ferroptosis and Pyroptosis Therapy Response Type A1 Journal article
  Year (down) 2022 Publication Antioxidants Abbreviated Journal Antioxidants  
  Volume 11 Issue 8 Pages 1548  
  Keywords A1 Journal article; Pharmacology. Therapy; Plasma Lab for Applications in Sustainability and Medicine – Antwerp (PLASMANT); Proteinscience, proteomics and epigenetic signaling (PPES)  
  Abstract Despite recent advances in melanoma treatment, there are still patients that either do not respond or develop resistance. This unresponsiveness and/or acquired resistance to therapy could be explained by the fact that some melanoma cells reside in a dedifferentiated state. Interestingly, this dedifferentiated state is associated with greater sensitivity to ferroptosis, a lipid peroxidation-reliant, iron-dependent form of cell death. Cytoglobin (CYGB) is an iron hexacoordinated globin that is highly enriched in melanocytes and frequently downregulated during melanomagenesis. In this study, we investigated the potential effect of CYGB on the cellular sensitivity towards (1S, 3R)-RAS-selective lethal small molecule (RSL3)-mediated ferroptosis in the G361 melanoma cells with abundant endogenous expression. Our findings show that an increased basal ROS level and higher degree of lipid peroxidation upon RSL3 treatment contribute to the increased sensitivity of CYGB knockdown G361 cells to ferroptosis. Furthermore, transcriptome analysis demonstrates the enrichment of multiple cancer malignancy pathways upon CYGB knockdown, supporting a tumor-suppressive role for CYGB. Remarkably, CYGB knockdown also triggers activation of the NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome and subsequent induction of pyroptosis target genes. Altogether, we show that silencing of CYGB expression modulates cancer therapy sensitivity via regulation of ferroptosis and pyroptosis cell death signaling pathways.  
  Address  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language Wos 000846411000001 Publication Date 2022-08-10  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 2076-3921 ISBN Additional Links UA library record; WoS full record; WoS citing articles  
  Impact Factor 7 Times cited Open Access OpenAccess  
  Notes Approved Most recent IF: 7  
  Call Number PLASMANT @ plasmant @c:irua:190686 Serial 7102  
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Author Van Loenhout, J.; Peeters, M.; Bogaerts, A.; Smits, E.; Deben, C. pdf  url
doi  openurl
  Title Oxidative Stress-Inducing Anticancer Therapies: Taking a Closer Look at Their Immunomodulating Effects Type A1 Journal article
  Year (down) 2020 Publication Antioxidants Abbreviated Journal Antioxidants  
  Volume 9 Issue 12 Pages 1188  
  Keywords A1 Journal article; Pharmacology. Therapy; Plasma Lab for Applications in Sustainability and Medicine – Antwerp (PLASMANT); Center for Oncological Research (CORE)  
  Abstract Cancer cells are characterized by higher levels of reactive oxygen species (ROS) compared to normal cells as a result of an imbalance between oxidants and antioxidants. However, cancer cells maintain their redox balance due to their high antioxidant capacity. Recently, a high level of oxidative stress is considered a novel target for anticancer therapy. This can be induced by increasing exogenous ROS and/or inhibiting the endogenous protective antioxidant system. Additionally, the immune system has been shown to be a significant ally in the fight against cancer. Since ROS levels are important to modulate the antitumor immune response, it is essential to consider the effects of oxidative stress-inducing treatments on this response. In this review, we provide an overview of the mechanistic cellular responses of cancer cells towards exogenous and endogenous ROS-inducing treatments, as well as the indirect and direct antitumoral immune effects, which can be both immunostimulatory and/or immunosuppressive. For future perspectives, there is a clear need for comprehensive investigations of different oxidative stress-inducing treatment strategies and their specific immunomodulating effects, since the effects cannot be generalized over different treatment modalities. It is essential to elucidate all these underlying immune effects to make oxidative stress-inducing treatments effective anticancer therapy.  
  Address  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language Wos 000602288600001 Publication Date 2020-11-27  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 2076-3921 ISBN Additional Links UA library record; WoS full record; WoS citing articles  
  Impact Factor 7 Times cited Open Access  
  Notes This research was funded by the Olivia Hendrickx Research Fund (21OCL06) and the University of Antwerp (FFB160231). Approved Most recent IF: 7; 2020 IF: NA  
  Call Number PLASMANT @ plasmant @c:irua:173865 Serial 6441  
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