The Role of <scp>PARP</scp>‐1 and <scp>NF‐κB</scp> in <scp>Bile‐Induced DNA</scp> Damage and Oncogenic Profile in Hypopharyngeal Cells

Doukas, Panagiotis G.; Vageli, Dimitra P.; Judson, Benjamin L.

doi:10.1002/lary.30284

Cited by 3 publications

(3 citation statements)

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“…Interestingly, in this study, no more severe DNA damage was observed in sh-PARP1 cells treated with HQ (Figure ). This phenomenon was also observed in a study conducted by Doukas PG et al on DNA damage caused by Bile . This may indicate that although knockdown PARP1 inhibits DNA damage caused by HQ through the PARP1 and NF-κB pathways, the attempt to regulate DNA damage through these pathways becomes meaningless because of the loss of the role of PARP1 in DNA damage repair.…”

Section: Discussionsupporting

confidence: 65%

“…This phenomenon was also observed in a study conducted by Doukas PG et al on DNA damage caused by Bile. 44 This may indicate that although knockdown PARP1 inhibits DNA damage caused by HQ through the PARP1 and NF-κB pathways, the attempt to regulate DNA damage through these pathways becomes meaningless because of the loss of the role of PARP1 in DNA damage repair. These results indicate that inappropriate inhibition of PARP1 is not beneficial for the repair of DNA damage caused by HQ and that appropriately activating PARP1 and inhibiting the NF-κB pathway can aid in DNA damage repair and cell survival.…”

Section: Discussionmentioning

confidence: 99%

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Role of the PARP1/NF-κB Pathway in DNA Damage and Apoptosis of TK6 Cells Induced by Hydroquinone

Wu,

Tang,

Zou

et al. 2024

Chem. Res. Toxicol.

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Hydroquinone(HQ) is a widely used industrial raw material and is a topical lightening product found in over-the-counter products. However, inappropriate exposure to HQ can pose certain health hazards. This study aims to explore the mechanisms of DNA damage and cell apoptosis caused by HQ, with a focus on whether HQ activates the nuclear factor-κB (NF-κB) pathway to participate in this process and to investigate the correlation between the NF-κB pathway activation and poly(ADP-ribose) polymerase 1(PARP1). Through various experimental techniques, such as DNA damage detection, cell apoptosis assessment, cell survival rate analysis, immunofluorescence, and nuclear-cytoplasmic separation, the cytotoxic effects of HQ were verified, and the activation of the NF-κB pathway was observed. Simultaneously, the relationship between the NF-κB pathway and PARP1 was verified by shRNA interference experiments. The results showed that HQ could significantly activate the NF-κB pathway, leading to a decreased cell survival rate, increased DNA damage, and cell apoptosis. Inhibiting the NF-κB pathway could significantly reduce HQ-induced DNA damage and cell apoptosis and restore cell proliferation and survival rate. shRNA interference experiments further indicated that the activation of the NF-κB pathway was regulated by PARP1. This study confirmed the important role of the NF-κB pathway in HQ-induced DNA damage and cell apoptosis and revealed that the activation of the NF-κB pathway was mediated by PARP1. This research provides important clues for a deeper understanding of the toxic mechanism of HQ.

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Section: Discussionsupporting

confidence: 65%

Section: Discussionmentioning

confidence: 99%

Role of the PARP1/NF-κB Pathway in DNA Damage and Apoptosis of TK6 Cells Induced by Hydroquinone

Wu,

Tang,

Zou

et al. 2024

Chem. Res. Toxicol.

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“…Interestingly, the saliva bile salt concentration was predictive of the severity of LPR [18]. The toxicity of bile salts on laryngopharyngeal tissue was confirmed in experimental studies that supported a potential carcinogenic role of bile acids in laryngeal squamous cell carcinoma [19]. According to the literature, pepsin and bile acids may be considered important etiological factors for upper aerodigestive tract mucosa inflammation and related symptoms and findings.…”

Section: Physiology 21 Gastroduodenal Enzymesmentioning

confidence: 81%

Personalized Treatments Based on Laryngopharyngeal Reflux Patient Profiles: A Narrative Review

Lechien

2023

JPM

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Objective: To review the current findings of the literature on the existence of several profiles of laryngopharyngeal reflux (LPR) patients and to propose personalized diagnostic and therapeutic approaches. Methods: A state-of-the art review of the literature was conducted using the PubMED, Scopus, and Cochrane Library databases. The information related to epidemiology, demographics, clinical presentations, diagnostic approaches, and therapeutic responses were extracted to identify outcomes that may influence the clinical and therapeutic courses of LPR. Results: The clinical presentation and therapeutic courses of LPR may be influenced by gender, age, weight, comorbidities, dietary habits and culture, anxiety, stress, and saliva enzyme profile. The clinical expression of reflux, including laryngopharyngeal, respiratory, nasal, and eye symptoms, and the hypopharyngeal–esophageal multichannel intraluminal impedance-pH monitoring profile of patients are important issues to improve in patient management. The use of more personalized therapeutic strategies appears to be associated with better symptom relief and cures over the long-term. The role of pepsin in LPR physiology is well-established but the lack of information about the role of other gastrointestinal enzymes in the development of LPR-related mucosa inflammation limits the development of future enzyme-based personalized diagnostic and therapeutic approaches. Conclusion: Laryngopharyngeal reflux is a challenging ear, nose, and throat condition associated with poor therapeutic responses and a long-term burden in Western countries. Artificial intelligence should be used for developing personalized therapeutic strategies based on patient features.

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Assessing the Impact of Gastroesophageal Reflux Disease on the Risk of Oral Cavity and Pharyngeal Cancer Using Mendelian Randomization

Wang,

Shen,

Cao

et al. 2023

Preprint

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Purpose: Previous observational studies have yielded inconsistent findings regarding the relationship between gastroesophageal reflux disease (GERD) and the risk of oral cavity and pharyngeal cancer (OCPC). This study aims to employ Mendelian randomization (MR) to explore whether a causal relationship exists between GERD and the risk of OCPC and its subtypes. Methods:Using summary data from genome-wide association studies (GWAS), we conducted MR analyses to assess the causal relationship between GERD and OCPC (comprising oral cavity cancer (OCC) and oropharynx cancer (OPC)). We performed univariable MR analyses with GERD as the exposure and OCPC, OCC, and OPC as outcomes. Cigarette smoking, alcohol consumption, body mass index (BMI), and type 2 diabetes (T2D) were adjusted for in the multivariable MR analysis to refine causal estimates. Results: Univariable MR analysis revealed that genetically predicted GERD increased the risk of OCPC (IVW: discovery, OR = 2.09, 95% CI: 1.30-3.37, P = 0.0023; validation, OR = 1.90, 95% CI: 1.26-2.87, P = 0.0020) and OCC (IVW: discovery, OR = 2.01, 95% CI: 1.21-3.33, P = 0.0066; validation: OR = 2.60, 95% CI: 1.47-4.59, P = 0.0010). The association between GERD and OPC was significant only in the discovery analysis (IVW: discovery, OR = 2.30, 95% CI: 1.08-4.89, P = 0.0307; validation: OR = 1.15, 95% CI: 0.67-1.97, P = 0.6199). Multivariable analysis, adjusting for smoking, alcohol, BMI, and T2D, produced consistent results. Conclusions: This MR study indicates a connection between GERD and an overall increased risk of OCPC. The association between GERD and OCC is also significant. This association is independent of CigDay, DrnkWk, BMI, and T2D. However, the link between GERD and OPC is limited and requires further investigation for confirmation. These findings could have significant public health implications and may aid in the prevention and treatment of oral and pharyngeal cancers. Exploring the specific mechanisms behind GERD increasing the risk of OCPC is necessary.

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The Role of PARP‐1 and NF‐κB in Bile‐Induced DNA Damage and Oncogenic Profile in Hypopharyngeal Cells

Cited by 3 publications

References 61 publications

Role of the PARP1/NF-κB Pathway in DNA Damage and Apoptosis of TK6 Cells Induced by Hydroquinone

Role of the PARP1/NF-κB Pathway in DNA Damage and Apoptosis of TK6 Cells Induced by Hydroquinone

Personalized Treatments Based on Laryngopharyngeal Reflux Patient Profiles: A Narrative Review

Assessing the Impact of Gastroesophageal Reflux Disease on the Risk of Oral Cavity and Pharyngeal Cancer Using Mendelian Randomization

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