Glutathione Peroxidase (GPx) and Superoxide Dismutase (SOD) in Oropharyngeal Cancer Associated with EBV and HPV Coinfection

Strycharz-Dudziak, Małgorzata; Fołtyn, Sylwia; Dworzański, Jakub; Kiełczykowska, Małgorzata; Malm, Maria; Drop, Bartłomiej; Polz‐Dacewicz, Małgorzata

doi:10.3390/v12091008

Cited by 25 publications

(19 citation statements)

References 42 publications

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“…Since no examples of actual photokilling were examined, it is not clear that these results reflect the role of PDT as a means to tumor eradication. Several studies have indicated that hypoxia can limit photokilling (14,15), indicating that ROS formation is required. Affinity of photosensitizing agents for sub‐cellular membranes is, however, a determinant of efficacy since ROS formed during irradiation will have a very limited lifetime.…”

Section: Discussionmentioning

confidence: 99%

“…These include decreased glucose metabolism and more dependence on mitochondrial respiration. There was also a report that infection with Epstein/Barr and HPV can lower both glutathione peroxidase and superoxide dismutase levels which would be expected to promote photokilling (15). No data were acquired from cells lacking both infections, so there the “base‐line” values were missing.…”

Section: Discussionmentioning

confidence: 99%

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Characteristics of an Impaired PDT Response

Kessel

Cho

Rakowski

et al. 2021

Photochem & Photobiology

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A concurrent human papilloma virus (HPV) infection potentiates the efficacy of ionizing radiation for treatment of head and neck cancer by promoting apoptosis. Studies in cell culture indicated an opposite effect for photodynamic therapy (PDT) when this leads to mitochondrial and ER photodamage. The explanation for this difference in PDT efficacy remains to be established. While apoptosis was impaired in HPV(‐) cells, such cells can be killed via photodamage directed at the ER: this leads to a nonapoptotic death pathway termed paraptosis. No differences in photosensitizer uptake or reactive oxygen species (ROS) production were observed in HPV(+) vs. HPV(‐) tumors. We now provide evidence that death pathways initiated by ER/mitochondrial photodamage leading to either paraptosis or apoptosis are impaired in an HPV(+) head and neck cell line. These results illustrate the complex determinants of PDT efficacy, a topic that has yet to be fully explored.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Characteristics of an Impaired PDT Response

Kessel

Cho

Rakowski

et al. 2021

Photochem & Photobiology

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“…In OPSCC, the activity of glutathione peroxidase (GPx) and superoxide dismutase (SOD) antioxidant enzymes was significantly decreased in patients with HPV/EBV coinfection when compared with HPV or EBV infection alone. A low GPx and SOD activity was observed in HPV/EBV-coinfected patients with poorly differentiated tumors and an advanced stage of disease [ 226 ].…”

Section: Possible Mechanisms Of Hr-hpv/ebv Cooperationmentioning

confidence: 99%

High-Risk Human Papillomavirus and Epstein–Barr Virus Coinfection: A Potential Role in Head and Neck Carcinogenesis

Blanco

Carrillo-Beltrán

Corvalán

et al. 2021

Biology

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High-risk human papillomaviruses (HR-HPVs) and Epstein–Barr virus (EBV) are recognized oncogenic viruses involved in the development of a subset of head and neck cancers (HNCs). HR-HPVs are etiologically associated with a subset of oropharyngeal carcinomas (OPCs), whereas EBV is a recognized etiological agent of undifferentiated nasopharyngeal carcinomas (NPCs). In this review, we address epidemiological and mechanistic evidence regarding a potential cooperation between HR-HPV and EBV for HNC development. Considering that: (1) both HR-HPV and EBV infections require cofactors for carcinogenesis; and (2) both oropharyngeal and oral epithelium can be directly exposed to carcinogens, such as alcohol or tobacco smoke, we hypothesize possible interaction mechanisms. The epidemiological and experimental evidence suggests that HR-HPV/EBV cooperation for developing a subset of HNCs is plausible and warrants further investigation.

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“…The analysis of GPx and SOD activity in head and neck tumor tissue samples showed significantly lower levels of antioxidant enzymes in low-grade tumors [ 105 ]. A similar situation was found in patients with gastric cancer [ 106 ], oropharyngeal squamous cell carcinoma [ 107 ], prostate cancer [ 108 ], bladder cancer [ 109 , 110 ], ovarian cancer [ 111 ], etc.…”

Section: Role Of Oxidative Stress In Cancer Progressionmentioning

confidence: 99%

Therapeutic Influence on Important Targets Associated with Chronic Inflammation and Oxidative Stress in Cancer Treatment

Neganova

Liu

Aleksandrova

et al. 2021

Cancers

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Chronic inflammation and oxidative stress are the interconnected pathological processes, which lead to cancer initiation and progression. The growing level of oxidative and inflammatory damage was shown to increase cancer severity and contribute to tumor spread. The overproduction of reactive oxygen species (ROS), which is associated with the reduced capacity of the endogenous cell defense mechanisms and/or metabolic imbalance, is the main contributor to oxidative stress. An abnormal level of ROS was defined as a predisposing factor for the cell transformation that could trigger pro-oncogenic signaling pathways, induce changes in gene expression, and facilitate accumulation of mutations, DNA damage, and genomic instability. Additionally, the activation of transcription factors caused by a prolonged oxidative stress, including NF-κB, p53, HIF1α, etc., leads to the expression of several genes responsible for inflammation. The resulting hyperactivation of inflammatory mediators, including TNFα, TGF-β, interleukins, and prostaglandins can contribute to the development of neoplasia. Pro-inflammatory cytokines were shown to trigger adaptive reactions and the acquisition of resistance by tumor cells to apoptosis, while promoting proliferation, invasion, and angiogenesis. Moreover, the chronic inflammatory response leads to the excessive production of free radicals, which further aggravate the initiated reactions. This review summarizes the recent data and progress in the discovery of mechanisms that associate oxidative stress and chronic inflammation with cancer onset and metastasis. In addition, the review provides insights for the development of therapeutic approaches and the discovery of natural substances that will be able to simultaneously inhibit several key oncological and inflammation-related targets.

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Glutathione Peroxidase (GPx) and Superoxide Dismutase (SOD) in Oropharyngeal Cancer Associated with EBV and HPV Coinfection

Cited by 25 publications

References 42 publications

Characteristics of an Impaired PDT Response

Characteristics of an Impaired PDT Response

High-Risk Human Papillomavirus and Epstein–Barr Virus Coinfection: A Potential Role in Head and Neck Carcinogenesis

Therapeutic Influence on Important Targets Associated with Chronic Inflammation and Oxidative Stress in Cancer Treatment

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