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成釉细胞瘤和牙源性角化囊肿中WT-1、Syndecan和Snail的免疫组织化学比较分析:一项回顾性研究

Comparative immunohistochemical analysis of WT-1, Syndecan and Snail in Ameloblastoma and odontogenic keratocyst: A retrospective study.

作者信息

Mukhopadhyay Arka, Panda Abikshyeet, Mishra Pallavi, Chowdhary Gopal, Mohanty Aishwariya, Sahoo Pravudeva D

机构信息

Department of Oral and Maxillofacial Pathology and Oral Microbiology, Hi-Tech Dental College and Hospital, Bhubaneswar, Odisha, India.

Department of Oral and Maxillofacial Pathology and Oral Microbiology, Kalinga Institute of Dental Sciences, KIIT Deemed to be University, Bhubaneswar, Odisha, India.

出版信息

J Oral Maxillofac Pathol. 2023 Apr-Jun;27(2):295-301. doi: 10.4103/jomfp.jomfp_301_22. Epub 2023 Jul 13.

DOI:10.4103/jomfp.jomfp_301_22
PMID:37854929
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10581317/
Abstract

BACKGROUND

The purpose of this experimental study was to evaluate and compare the degree of expression of Wilm's Tumor Gene-1 (WT-1), Syndecan (CD 138) and Snail in Ameloblastoma and odontogenic keratocyst (OKC) and to analyse their potential role in pathogenesis.

METHODS AND MATERIAL

Immunohistochemical analysis was performed to evaluate WT-1, Syndecan and Snail expression in Ameloblastoma ( = 20) and OKC ( = 20). Topographical immunoexpression pattern of Ameloblast-like cells, Stellate Reticulum-like cells in Ameloblastoma and basal layer as well as suprabasal layer of cells of OKC were also compared. The results obtained were subjected to ANOVA test and Tukey HSD test through SPSS software 20.0 for Microsoft Windows.

RESULTS

WT-1 and Snail overexpression was seen in both Ameloblastoma and OKCs. Syndecan, responsible for maintaining normal cellular morphology, cell-cell adhesion and differentiation was significantly downregulated in both the lesions. The Ameloblasts-like cells and the basal cells showed significantly higher immunopositivity for WT-1 and Syndecan as compared to that of basal cells. An inverse relation was noted for Snail protein. The ANOVA test predicted a statistically significant difference of expression across the lesions with a value <0.0001 for Syndecan and Snail.

CONCLUSIONS

The under-expression of epithelial membrane protein Syndecan-1 and upregulation of EMT transcription factor Snail can promote local invasion and is indicative of poor prognosis of these lesions. The overexpression of WT-1 results in tumorigenesis, proliferation and localized aggressiveness of Ameloblastoma and intrabony growth of OKC. Further investigation on the biologic behaviour of OKC is still recommended to arrive at more specific conclusions regarding its nature.

摘要

背景

本实验研究旨在评估和比较肾母细胞瘤基因-1(WT-1)、多配体蛋白聚糖(CD 138)和Snail在成釉细胞瘤和牙源性角化囊肿(OKC)中的表达程度,并分析它们在发病机制中的潜在作用。

方法与材料

采用免疫组织化学分析评估成釉细胞瘤(n = 20)和OKC(n = 20)中WT-1、多配体蛋白聚糖和Snail的表达。还比较了成釉细胞瘤中类似成釉细胞的细胞、星网状细胞以及OKC细胞的基底层和基底上层的免疫表达模式。通过适用于Microsoft Windows的SPSS软件20.0对所得结果进行方差分析和Tukey HSD检验。

结果

在成釉细胞瘤和OKC中均观察到WT-1和Snail的过表达。负责维持正常细胞形态、细胞间黏附和分化的多配体蛋白聚糖在两种病变中均显著下调。与基底细胞相比,类似成釉细胞的细胞和基底细胞对WT-1和多配体蛋白聚糖的免疫阳性率显著更高。Snail蛋白呈负相关。方差分析预测,各病变间的表达存在统计学显著差异,多配体蛋白聚糖和Snail的P值<0.0001。

结论

上皮膜蛋白多配体蛋白聚糖-1的低表达和上皮-间质转化转录因子Snail的上调可促进局部侵袭,并提示这些病变预后不良。WT-1的过表达导致成釉细胞瘤的肿瘤发生、增殖和局部侵袭性以及OKC的骨内生长。仍建议对OKC的生物学行为进行进一步研究,以得出关于其性质的更具体结论。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2df3/10581317/18dc7c775d7c/JOMFP-27-295-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2df3/10581317/c37b6e0b9a54/JOMFP-27-295-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2df3/10581317/8ec11d2e770f/JOMFP-27-295-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2df3/10581317/2b34cc9d2bf2/JOMFP-27-295-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2df3/10581317/07c819a0538e/JOMFP-27-295-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2df3/10581317/18dc7c775d7c/JOMFP-27-295-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2df3/10581317/c37b6e0b9a54/JOMFP-27-295-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2df3/10581317/8ec11d2e770f/JOMFP-27-295-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2df3/10581317/2b34cc9d2bf2/JOMFP-27-295-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2df3/10581317/07c819a0538e/JOMFP-27-295-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2df3/10581317/18dc7c775d7c/JOMFP-27-295-g005.jpg

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J Oral Sci. 2016;58(3):407-13. doi: 10.2334/josnusd.15-0546.
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