Localization of beta catenin across the domain of odontogenic lesions: A systematic review

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS ACS Applied Bio Materials Pub Date : 2023-10-15 DOI:10.1111/jop.13487
Shreya Chatterjee, Anju Devi, Mala Kamboj, Anjali Narwal
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Abstract

BACKGROUND CTNNB1 gene encodes beta catenin, a transcriptional activator of Wnt pathway involved in the pathogenesis of odontogenic lesions. Though located intramembranously, its translocation into cytoplasm and nucleus could trigger cell proliferation, inhibition of apoptosis, invasion and migration of the tumour cell. MATERIALS AND METHODS Five electronic databases including MEDLINE by PubMed, Google scholar, Scopus, Trip, Cochrane library and EMBASE until 1 January 2023 without period restriction were thoroughly searched. Those articles that identified CTNNB1 mutation and beta catenin in odontogenic lesions were included for review. Risk of bias was analysed for each study using QUADAS 2 tool and Review Manager 5.3 was used to output its result. RESULTS Thirty four published articles were included for data synthesis. A total of 1092 cases of odontogenic lesions were assessed for both CTNNB1 mutation and beta catenin expression. CTNNB1 mutation was observed in ameloblastoma, calcifying odontogenic cyst, calcifying cystic odontogenic tumour and all malignant odontogenic tumours. The beta catenin expression (nuclear and cytoplasmic) was maximum in odontogenic keratocyst and calcifying odontogenic cyst. The expression was variable in ameloblastomas, membranous in odontomas, calcifying cystic odontogenic tumour and nuclear in all malignant tumours. DISCUSSION AND CONCLUSION High recurrence of odontogenic keratocyst and aggressiveness of solid ameloblastoma and malignant odontogenic tumours could be associated with the nuclear translocation of beta catenin. Disparity between CTNNB1 mutation and beta catenin expression within odontogenic lesions suggests alternate routes of beta catenin activation. The review results support the unique localisation of beta catenin as a helpful diagnostic factor in the pathogenesis of odontogenic lesions.
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β-连环蛋白在牙源性病变中的定位:一项系统综述。
背景:CTNNB1基因编码β-连环蛋白,一种参与牙源性病变发病机制的Wnt通路转录激活因子。虽然位于膜内,但其向细胞质和细胞核的移位可以触发细胞增殖、抑制细胞凋亡、肿瘤细胞的侵袭和迁移。材料和方法:对PubMed的MEDLINE、Google scholar、Scopus、Trip、Cochrane library和EMBASE五个电子数据库进行了彻底搜索,直到2023年1月1日,没有时间限制。那些在牙源性病变中发现CTNNB1突变和β-连环蛋白的文章被纳入综述。使用QUADAS 2工具分析每项研究的偏倚风险,并使用Review Manager 5.3输出其结果。结果:34篇已发表的文章被纳入数据综合。对1092例牙源性病变的CTNNB1突变和β-连环蛋白表达进行了评估。在成釉细胞瘤、钙化性牙源性囊肿、钙化性囊性牙源性肿瘤和所有恶性牙源性肿瘤中观察到CTNNB1突变。β-连环蛋白在牙源性角化囊肿和钙化性牙源性囊肿中的表达(细胞核和细胞质)最高。成釉细胞瘤、成牙本质瘤、钙化性囊性牙源性肿瘤和所有恶性肿瘤的细胞核中的表达是可变的。讨论和结论:牙源性角化囊肿的高复发率、实体性成釉细胞瘤和牙源性恶性肿瘤的侵袭性可能与β-连环蛋白的核转位有关。牙源性病变中CTNNB1突变和β-连环蛋白表达之间的差异表明β-连环素激活的替代途径。综述结果支持β-连环蛋白作为一种有助于诊断牙源性病变发病机制的因素的独特定位。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
ACS Applied Bio Materials
ACS Applied Bio Materials Chemistry-Chemistry (all)
CiteScore
9.40
自引率
2.10%
发文量
464
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