Epigenetic Alterations and Inflammation as Emerging Use for the Advancement of Treatment in Non-Small Cell Lung Cancer

Yang, Shuo; Huang, Youliang; Zhao, Qi

doi:10.3389/fimmu.2022.878740

Cited by 21 publications

(14 citation statements)

References 227 publications

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“…Importantly, we determined that these effects and their progressive disappearance were associated with a size-dependent lung clearance of the GO materials [ 26 ]. However, long-lasting inflammation such as the one observed with micrometric GO [ 26 ] has been previously associated with an increased risk of developing cancer [ 31 ]. There is therefore a need to evaluate the potential of these micrometric materials to cause genotoxicity after chronic exposure, and the possible link between inflammation and DNA damage.…”

Section: Introductionmentioning

confidence: 99%

Lung recovery from DNA damage induced by graphene oxide is dependent on size, dose and inflammation profile

et al. 2022

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Background A key aspect of any new material safety assessment is the evaluation of their in vivo genotoxicity. Graphene oxide (GO) has been studied for many promising applications, but there are remaining concerns about its safety profile, especially after inhalation. Herein we tested whether GO lateral dimension, comparing micrometric (LGO) and nanometric (USGO) GO sheets, has a role in the formation of DNA double strand breaks in mouse lungs. We used spatial resolution and differential cell type analysis to measure DNA damages in both epithelial and immune cells, after either single or repeated exposure. Results GO induced DNA damages were size and dose dependent, in both exposure scenario. After single exposure to a high dose, both USGO and LGO induced significant DNA damage in the lung parenchyma, but only during the acute phase response (p < 0.05 for USGO; p < 0.01 for LGO). This was followed by a fast lung recovery at day 7 and 28 for both GOs. When evaluating the chronic impact of GO after repeated exposure, only a high dose of LGO induced long-term DNA damages in lung alveolar epithelia (at 84 days, p < 0.05). Regardless of size, low dose GO did not induce any significant DNA damage after repeated exposure. A multiparametric correlation analysis of our repeated exposure data revealed that transient or persistent inflammation and oxidative stress were associated to either recovery or persistent DNA damages. For USGO, recovery from DNA damage was correlated to efficient recovery from acute inflammation (i.e., significant secretion of SAA3, p < 0.001; infiltration of neutrophils, p < 0.01). In contrast, the persistence of LGO in lungs was associated to a long-lasting presence of multinucleated macrophages (up to 84 days, p < 0.05), an underlying inflammation (IL-1α secretion up to 28 days, p < 0.05) and the presence of persistent DNA damages at 84 days. Conclusions Overall these results highlight the importance of the exposure scenario used. We showed that LGO was more genotoxic after repeated exposure than single exposure due to persistent lung inflammation. These findings are important in the context of human health risk assessment and toward establishing recommendations for a safe use of graphene based materials in the workplace.

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Section: Introductionmentioning

confidence: 99%

Lung recovery from DNA damage induced by graphene oxide is dependent on size, dose and inflammation profile

et al. 2022

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“…In recent years, epigenetic modification has been widely studied. Existing evidence shows that epigenetic modification exists in various molecular biological processes, and it has a significant role in the occurrence and development of cancer 27 – 31 . As the more critical one, m 6 A RNA modification has also been shown to have an important direct relationship with cancers 32 – 36 .…”

Section: Discussionmentioning

confidence: 99%

Gene signature of m6A RNA regulators in diagnosis, prognosis, treatment, and immune microenvironment for cervical cancer

Wang

Ding

Wang

et al. 2022

Sci Rep

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Continuing studies imply that m6A RNA modification is involved in the development of cervical cancer (CC), but lack strong support on recurrence and diagnosis prediction. In this research, a comprehensive analysis of 33 m6A regulators was performed to fulfill them. Here, we performed diagnostic and prognosis models and identified key regulators, respectively. Then the CC patients were separated into two clusters in accordance with 33 regulators, and participants in the cluster 1 had a worse prognosis. Subsequently, the m6AScore was calculated to quantify the m6A modification pattern based on regulators and we found that patients in cluster 1 had higher m6AScore. Afterwards, immune microenvironment, cell infiltration, escape analyses and tumor burden mutation analyses were executed, and results showed that m6AScore was correlated with them, but to a limited extent. Interestingly, HLAs and immune checkpoint expression, and immunophenoscore in patients with high-m6AScores were significantly lower than those in the low-m6AScore group. These suggested the m6AScores might be used to predict the feasibility of immunotherapy in patients. Results provided a distinctive perspective on m6A modification and theoretical basis for CC diagnosis, prognosis, clinical treatment strategies, and potential mechanism exploration.

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“…Of note, aberrant inflammation has been extensively involved in many pulmonary diseases [ 7 ]. Similarly, treatments aimed at resolving inflammation function as a key contributor to the re-establishment of organismal homeostasis in many pulmonary diseases [ 6 , 7 , 21 , 22 ].…”

Section: Introductionmentioning

confidence: 99%

Hydrogen Sulfide: A Gaseous Mediator and Its Key Role in Programmed Cell Death, Oxidative Stress, Inflammation and Pulmonary Disease

2022

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Hydrogen sulfide (H2S) has been acknowledged as a novel gaseous mediator. The metabolism of H2S in mammals is tightly controlled and is mainly achieved by many physiological reactions catalyzed by a suite of enzymes. Although the precise actions of H2S in regulating programmed cell death, oxidative stress and inflammation are yet to be fully understood, it is becoming increasingly clear that H2S is extensively involved in these crucial processes. Since programmed cell death, oxidative stress and inflammation have been demonstrated as three important mechanisms participating in the pathogenesis of various pulmonary diseases, it can be inferred that aberrant H2S metabolism also functions as a critical contributor to pulmonary diseases, which has also been extensively investigated. In the meantime, substantial attention has been paid to developing therapeutic approaches targeting H2S for pulmonary diseases. In this review, we summarize the cutting-edge knowledge on the metabolism of H2S and the relevance of H2S to programmed cell death, oxidative stress and inflammation. We also provide an update on the crucial roles played by H2S in the pathogenesis of several pulmonary diseases. Finally, we discuss the perspective on targeting H2S metabolism in the treatment of pulmonary diseases.

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Epigenetic Alterations and Inflammation as Emerging Use for the Advancement of Treatment in Non-Small Cell Lung Cancer

Cited by 21 publications

References 227 publications

Lung recovery from DNA damage induced by graphene oxide is dependent on size, dose and inflammation profile

Lung recovery from DNA damage induced by graphene oxide is dependent on size, dose and inflammation profile

Gene signature of m6A RNA regulators in diagnosis, prognosis, treatment, and immune microenvironment for cervical cancer

Hydrogen Sulfide: A Gaseous Mediator and Its Key Role in Programmed Cell Death, Oxidative Stress, Inflammation and Pulmonary Disease

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