关键词: ameloblastoma local aggressiveness odontogenic tumour proteomics recurrence

Mesh : Humans Ameloblastoma / genetics pathology Dentigerous Cyst / genetics pathology Proteomics Odontogenic Cysts / genetics Odontogenic Tumors / genetics

来  源:   DOI:10.1111/jop.13433

Abstract:
BACKGROUND: Reports on the proteomic studies of ameloblastoma and other common odontogenic lesions are limited. We thus explored the differential proteins among ameloblastoma, odontogenic keratocyst, dentigerous cyst, and normal gingival tissue using proteomics and identified hub proteins involved in the local aggressiveness and recurrence of ameloblastoma.
METHODS: Samples were obtained from 14 patients with ameloblastoma, 6 with odontogenic keratocyst, 9 with a dentigerous cyst, and 5 with normal gingival tissue. Proteins were then extracted, purified, quantified, and analysed using Easy-nLC chromatography and mass spectrometry. Further functional annotation and enrichment analyses were performed using Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes on the target protein collection. Protein clustering and protein-protein interaction network analyses were used to screen the hub proteins. Proteins with significant interactions were screened according to their degree index. These results were verified by immunohistochemical staining. Proteins meeting the screening criteria of expression difference ploidy >1.2-fold (upregulation and downregulation) and p < 0.05 were considered differential proteins.
RESULTS: In ameloblastoma, 808 differential proteins were upregulated and 505 were downregulated compared with those in odontogenic keratocyst; 309 were upregulated and 453 were downregulated compared with those in dentigerous cyst; and 2210 were upregulated and 829 were downregulated compared with those in normal gingival tissue. The three groups of differential proteins were associated with cellular exosomes, antigen binding, complement activation, human papillomavirus infection, focal adhesion, cell adhesion molecules, and metabolic pathways.
CONCLUSIONS: CDH3 is associated with the local aggressiveness and recurrence of ameloblastoma and is a potential therapeutic target.
摘要:
背景:成釉细胞瘤和其他常见牙源性病变的蛋白质组学研究报道有限。因此,我们探索了成釉细胞瘤之间的差异蛋白,牙源性角化囊肿,牙质囊肿,和正常牙龈组织使用蛋白质组学和鉴定hub蛋白参与成釉细胞瘤的局部侵袭性和复发。
方法:从14例成釉细胞瘤患者中获取样本,6患有牙源性角化囊肿,9有牙质囊肿,和5个正常牙龈组织。然后提取蛋白质,纯化,量化,并使用Easy-nLC色谱和质谱进行分析。使用基因本体论和京都基因和基因组百科全书对靶蛋白集合进行进一步的功能注释和富集分析。蛋白质聚类和蛋白质-蛋白质相互作用网络分析用于筛选hub蛋白。根据程度指数筛选具有显著相互作用的蛋白质。这些结果通过免疫组织化学染色证实。满足表达差异倍性>1.2倍(上调和下调)和p<0.05的筛选标准的蛋白质被认为是差异蛋白质。
结果:成釉细胞瘤,与牙源性角化囊肿相比,808种差异蛋白上调,505种下调;与牙源性角化囊肿相比,309种上调,453种下调;与正常牙龈组织相比,2210种上调,829种下调。三组差异蛋白与细胞外泌体相关,抗原结合,补体激活,人乳头瘤病毒感染,病灶粘连,细胞粘附分子,和代谢途径。
结论:CDH3与成釉细胞瘤的局部侵袭性和复发相关,是一个潜在的治疗靶点。
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