Stratifin in ocular surface squamous neoplasia and its association with p53.
14-3-3 Proteins
/ biosynthesis
Adolescent
Adult
Aged
Aged, 80 and over
Biomarkers, Tumor
/ genetics
Carcinoma, Squamous Cell
/ diagnosis
Child
Conjunctival Neoplasms
/ diagnosis
DNA Mutational Analysis
DNA, Neoplasm
/ genetics
Exoribonucleases
/ biosynthesis
Female
Gene Expression Regulation
Humans
Male
Middle Aged
Mutation
Neoplasm Staging
Tumor Suppressor Protein p53
/ biosynthesis
Young Adult
immunohistochemistry
methylation-specific PCR
ocular surface squamous neoplasia (OSSN)
p53
reverse transcription PCR
stratifin
Journal
Acta ophthalmologica
ISSN: 1755-3768
Titre abrégé: Acta Ophthalmol
Pays: England
ID NLM: 101468102
Informations de publication
Date de publication:
Dec 2021
Dec 2021
Historique:
received:
17
06
2020
accepted:
23
02
2021
pubmed:
27
3
2021
medline:
15
1
2022
entrez:
26
3
2021
Statut:
ppublish
Résumé
Sunlight-induced p53 mutations are known to contribute towards increased risk of ocular surface squamous neoplasia (OSSN). Stratifin (14-3-3σ)/HEM (human epithelial marker) is a p53-mediated inhibitor of cell cycle progression and has been shown to be a target of epigenetic deregulation in various carcinomas. In the present study, Stratifin expression, its promoter methylation status as well as expression of mutant p53 in early and advanced AJCC stages (8th edition) of OSSN, was evaluated. Sixty-four OSSN [20 conjunctival intraepithelial neoplasia (CIN) and 44 squamous cell carcinoma (SCC)] patients were registered for this study, and they were followed up for 36-58 months (mean 48 ± 3.6). Immunoexpression of Stratifin and mutant p53 protein, mRNA expression of Stratifin by reverse transcription polymerase chain reaction (PCR) and methylation status of Stratifin by methylation-specific PCR, was undertaken. Hypermethylation of Stratifin promoter in 63% (40/64), loss of Stratifin expression in 75% (48/64) and downregulation of Stratifin mRNA in 61% (39/64) were observed. Stratifin hypermethylation was significantly associated with reduced disease-free survival in both early and advanced T stage SCC cases. Expression of mutant p53 expression was seen in 48% (31/64) OSSN cases. Of the 31 patients with mutant p53 expression, 87% (27/31) also demonstrated loss of Stratifin immunoexpression. A significant association was seen between mutant p53 expression and Stratifin loss (p = 0.01) in advanced T stage SCC cases. Hypermethylation of Stratifin gene and its reduced mRNA expression both are potential biomarkers for identifying high-risk OSSN patients. Aberrant methylation of Stratifin and simultaneous mutant p53 expression implicates involvement of p53-Stratifin mediated signalling pathway in the pathogenesis of OSSN.
Substances chimiques
14-3-3 Proteins
0
Biomarkers, Tumor
0
DNA, Neoplasm
0
TP53 protein, human
0
Tumor Suppressor Protein p53
0
Exoribonucleases
EC 3.1.-
SFN protein, human
EC 3.1.-
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e1483-e1491Subventions
Organisme : Indian Council of Medical Research, New Delhi
ID : 2006-09-11
Informations de copyright
© 2021 Acta Ophthalmologica Scandinavica Foundation. Published by John Wiley & Sons Ltd.
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