p53 polymorphism and association of human papillomavirus in oral submucous fibrosis and oral squamous cell carcinoma: A case–control study

Hallikeri, Kaverı; Burde, Krishna; Anehosur, Venktesh; Kulkarni, Bhushan; Hiremath, Shivaprakash V.

doi:10.4103/jomfp.jomfp_180_18

Cited by 8 publications

(4 citation statements)

References 32 publications

(48 reference statements)

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“… 47 In addition, the p53 codon 72 polymorphism is predominantly observed as Arginine/Arginine protein in the control group, OSF group, and OSCC group, followed by Proline/Proline and Arginine/Proline proteins. 48 These findings suggest that amino acids were involved in protein synthesis-mediated disease progression of OSF. Furthermore, recent studies have confirmed that local photodynamic therapy using 5-aminolevulinic acid was safe and effective for the treatment of oral leukoplakia combined with OSF, but long-term follow-up was required.…”

Section: Discussionmentioning

confidence: 89%

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Jiawei Danxuan Koukang Alleviates Arecoline Induced Oral Mucosal Lesions: Network Pharmacology and the Combined Ultra-High Performance Liquid Chromatography (UPLC) and Mass Spectrometry (MS)

Zhou,

Tan,

Dai

et al. 2023

DDDT

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Purpose Arecoline is one of the main toxic components of arecoline to cause oral mucosal lesions or canceration, which seriously affects the survival and life quality of patients. This study analyzed the mechanism of Jiawei Danxuan Koukang (JDK) in alleviating arecoline induced oral mucosal lesions, to provide new insights for the treatment of oral submucosal fibrosis (OSF) or cancerosis. Methods Metabolomics was applied to analyze the composition of JDK and serum metabolites. The active ingredients of JDK were analyzed by the combined ultra-high performance liquid chromatography and mass spectrometry. The target network of JDK, metabolites and OSF was analyzed by network pharmacology, and molecular docking. Oral mucosal lesions and fibrosis were analyzed by HE and Masson staining. Cell differentiation, proliferation and apoptosis were detected. The expressions of α-SMA, Collagen I, Vimentin, Snail, E-cadherin, AR and NOTCH1 were detected by Western blot. Results Arecoline induced the gradual atrophy and thinning of rat oral mucosal, collagen accumulation, the increase expressions of fibrosis-related proteins and Th17/Treg ratio. JDK inhibited arecoline-induced oral mucosal lesions and inflammatory infiltration. Arecoline induced changes of serum metabolites in Aminoacyl-tRNA biosynthesis, Alanine, aspartate and glutamate metabolism and Arginine biosynthesis pathways, which were reversed by M-JDK. Quercetin and AR were the active ingredients and key targets of JDK, metabolites and OSF interaction. Arecoline promoted the expression of AR protein, and the proliferation of oral fibroblasts. Quercetin inhibited the effect of arecoline on oral fibroblasts, but was reversed by AR overexpression. Arecoline induced NOTCH1 expression in CAL27 and SCC-25 cells, and promoted cell proliferation, but was reversed by M-JDK or quercetin. Conclusion JDK improved the arecoline-induced OSF and serum metabolite functional pathway. Quercetin targeted AR protein to improve arecoline-induced OSF. JDK and quercetin inhibited arecoline-induced NOTCH1 protein expression in CAL27 and SCC-25 cells to play an anti-oral cancer role.

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Section: Discussionmentioning

confidence: 89%

Section: Discussionmentioning

confidence: 95%

Jiawei Danxuan Koukang Alleviates Arecoline Induced Oral Mucosal Lesions: Network Pharmacology and the Combined Ultra-High Performance Liquid Chromatography (UPLC) and Mass Spectrometry (MS)

Zhou,

Tan,

Dai

et al. 2023

DDDT

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“…HPV type 16 in the human cell causes the synthesis of two oncoproteins called E6 and E7. These two oncoproteins are capable of altering the physiological function of p53 and RB1 increasing the possibility of causing lesions in the oral epithelial cells [28][29][30].…”

Section: Oral Squamous Carcinoma and Oral Potentially Malignant Disor...mentioning

confidence: 99%

Chemopreventive and Biological Strategies in the Management of Oral Potentially Malignant and Malignant Disorders

Viglianisi,

Polizzi,

Grippaudo

et al. 2024

Bioengineering

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Oral potentially malignant disorders (OPMD) and oral squamous cell carcinoma (OSCC) represent a significant global health burden due to their potential for malignant transformation and the challenges associated with their diagnosis and treatment. Chemoprevention, an innovative approach aimed at halting or reversing the neoplastic process before full malignancy, has emerged as a promising avenue for mitigating the impact of OPMD and OSCC. The pivotal role of chemopreventive strategies is underscored by the need for effective interventions that go beyond traditional therapies. In this regard, chemopreventive agents offer a unique opportunity to intercept disease progression by targeting the molecular pathways implicated in carcinogenesis. Natural compounds, such as curcumin, green tea polyphenols, and resveratrol, exhibit anti-inflammatory, antioxidant, and anti-cancer properties that could make them potential candidates for curtailing the transformation of OPMD to OSCC. Moreover, targeted therapies directed at specific molecular alterations hold promise in disrupting the signaling cascades driving OSCC growth. Immunomodulatory agents, like immune checkpoint inhibitors, are gaining attention for their potential to harness the body’s immune response against early malignancies, thus impeding OSCC advancement. Additionally, nutritional interventions and topical formulations of chemopreventive agents offer localized strategies for preventing carcinogenesis in the oral cavity. The challenge lies in optimizing these strategies for efficacy, safety, and patient compliance. This review presents an up to date on the dynamic interplay between molecular insights, clinical interventions, and the broader goal of reducing the burden of oral malignancies. As research progresses, the synergy between early diagnosis, non-invasive biomarker identification, and chemopreventive therapy is poised to reshape the landscape of OPMD and OSCC management, offering a glimpse of a future where these diseases are no longer insurmountable challenges but rather preventable and manageable conditions.

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“…Base on the above process and the ow diagram of the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guideline (supplementary Figure S1), 13 eligible case-control studies on TP53 codon 72 polymorphism and OPMD onset or progression were retrieved for detailed evaluation from the literature databases (Table 1). [14][15][16][17][18][19][20][21][22][23][24][25][26] Table 1 The characteristics of the included case-control studies on p53 protein codon 72 polymorphism in onset and progression of OPMD…”

Section: Search Strategy and Data Extractionmentioning

confidence: 99%

Evaluation of associations between TP53 codon 72 polymorphism and onset and progression of oral potentially malignant disorders based on case-control studies

Zhou

Liu

Yang

et al. 2023

Preprint

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Background Recently, a systematic review and meta-analysis demonstrated that overexpression of p53 immunoprotein was significantly associated with progression risk of oral potentially malignant disorders (OPMD). However, the results of investigations on TP53 genetic typing in OPMD were inconsistent and inconclusive. Methods A systematic evaluation was conducted to identify all eligible case-control studies on the associations between TP53 codon 72 polymorphism and both onset and progression of OPMD. Results A total of 768 OPMD patients and 1173 healthy individuals were identified from 12 eligible case-control studies on TP53 codon 72 polymorphism OPMD onset. In overall and subgroup analyses, no significantly risk of OPMD onset was observed in the cases for genetic models including allele C vs. G, homozygote CC vs. GG, heterozygote GC vs. GG, dominant GC + CC vs. GG, and recessive CC vs. GG + GC (all P-value of association test > 0.05). Further, a total of 465 OPMD patients and 775 oral squamous cell carcinoma (OSCC) ones were identified from 8 eligible case-control studies on this polymorphism in OPMD progression to OSCC. The analyses revealed that there was also no significantly risk of OPMD progression in the cases for the genetic models (all P-value of association test > 0.05). Conclusion Our data of a pooled-analysis indicates that TP53 codon 72 polymorphism may not act as genetic factor for the risk of OPMD onset and progression. Combined with the conclusion by a systematic review and meta-analysis, we put forward a new opinion that TP53 genetic typing cloud not influence p53 protein expression in OPMD.

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p53 polymorphism and association of human papillomavirus in oral submucous fibrosis and oral squamous cell carcinoma: A case–control study

Cited by 8 publications

References 32 publications

Jiawei Danxuan Koukang Alleviates Arecoline Induced Oral Mucosal Lesions: Network Pharmacology and the Combined Ultra-High Performance Liquid Chromatography (UPLC) and Mass Spectrometry (MS)

Jiawei Danxuan Koukang Alleviates Arecoline Induced Oral Mucosal Lesions: Network Pharmacology and the Combined Ultra-High Performance Liquid Chromatography (UPLC) and Mass Spectrometry (MS)

Chemopreventive and Biological Strategies in the Management of Oral Potentially Malignant and Malignant Disorders

Evaluation of associations between TP53 codon 72 polymorphism and onset and progression of oral potentially malignant disorders based on case-control studies

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