| Records |
| Author |
De Backer, J.; Maric, D.; Zuhra, K.; Bogaerts, A.; Szabo, C.; Vanden Berghe, W.; Hoogewijs, D. |
| Title |
Cytoglobin Silencing Promotes Melanoma Malignancy but Sensitizes for Ferroptosis and Pyroptosis Therapy Response |
Type |
A1 Journal article |
Year  |
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 |
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| Corporate Author |
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Thesis |
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| Publisher |
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Place of Publication |
|
Editor |
|
| Language |
|
Wos |
000846411000001 |
Publication Date |
2022-08-10 |
| Series Editor |
|
Series Title |
|
Abbreviated Series Title |
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| 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 |
| Permanent link to this record |
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| Author |
Van Loenhout, J.; Peeters, M.; Bogaerts, A.; Smits, E.; Deben, C. |
| Title |
Oxidative Stress-Inducing Anticancer Therapies: Taking a Closer Look at Their Immunomodulating Effects |
Type |
A1 Journal article |
| Year |
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 |
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| Corporate Author |
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Thesis |
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| 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 |
| Permanent link to this record |
