Research Progress of EMR2 Receptor Function in Glioma and its Potential Application as Therapeutic Target.

Current health sciences journal Pub Date : 2024-10-01 Epub Date: 2024-12-31 DOI:10.12865/CHSJ.50.04.02
Iuliana Mihaela Buzatu, Alexandra Costachi, Anca Oana Docea, Elena Victoria Manea, Ovidiu Zlatian
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Abstract

The most frequent primary brain malignancy is glioma. Alterations in several adhesion G-protein-coupled receptors (aGPCRs) are present in cancer as they regulate adhesion, migration, and guidance. Epidermal growth factor (EGF) module-containing mucin-like receptor 2 (EMR2) is included in group II GPCRs and functionally in a family of brain angiogenesis inhibitor molecules (BAIs). Recent studies have shown that BAIs regulate phagocytosis and synaptogenesis, and their extracellular domain inhibits angiogenesis and tumor growth. In neoplastic processes, EMR2 appears to play a role in disease aggressiveness, patient survival rates, and tumor grade. This review summarizes the EMR2 involvement in cellular mechanisms and pathologies, particularly in cancer. We searched the Pubmed Central, Google Scholar and Scopus databases for terms "EMR2" and "glioma". The initial search yielded a total of 92 results. After excluding studies not written in English, based on design, and excluding duplicates and non-relevant studies, we included 38 studies in the review. EMR2 was shown to be expressed in various histologic grades of gliomas and to be linked to the PI3K pathway, as both are upregulated in glioblastoma after bevacizumab therapy. The PI3K-Akt pathway is involved in tumorigenesis, and upregulation of EMR2 may in turn upregulate PI3K, leading to increased tumor invasiveness. Indeed, overexpression of EMR2 was associated with the mesenchymal glioblastoma subtype, tumor invasiveness, and poor survival. EMR2 also regulates neutrophil function by producing reactive oxygen species (ROS) and degranulation. Possible therapeutic approaches have been studied, such as the stimulation of microglia and monocytes to inhibit tumor-initiating cells by down-regulating the EMR2 gene or through an antibody against EMR2. The current review summarizes the knowledge about the EMR2 receptor that can serve as motivation for future studies on its role in the clinical evolution and tumor biology of gliomas in order to find new modulator therapeutic approaches.

EMR2受体在胶质瘤中的作用及其作为治疗靶点的研究进展。
最常见的原发性脑恶性肿瘤是神经胶质瘤。一些粘附g蛋白偶联受体(agpcr)的改变存在于癌症中,因为它们调节粘附、迁移和引导。含有表皮生长因子(EGF)模块的粘蛋白样受体2 (EMR2)被纳入II组gpcr,并在功能上属于脑血管生成抑制剂分子(BAIs)家族。最近的研究表明BAIs调节吞噬和突触发生,其胞外结构域抑制血管生成和肿瘤生长。在肿瘤过程中,EMR2似乎在疾病侵袭性、患者生存率和肿瘤分级中发挥作用。本文综述了EMR2在细胞机制和病理中的作用,特别是在癌症中的作用。我们在Pubmed Central、谷歌Scholar和Scopus数据库中搜索“EMR2”和“glioma”。最初的搜索总共产生了92个结果。在基于设计排除非英文研究、重复研究和非相关研究后,我们纳入了38项研究。EMR2在不同组织学级别的胶质瘤中表达,并与PI3K通路相关,因为在贝伐单抗治疗后,两者在胶质母细胞瘤中上调。PI3K- akt通路参与肿瘤发生,EMR2的上调可能反过来上调PI3K,导致肿瘤侵袭性增加。事实上,EMR2的过表达与间充质胶质母细胞瘤亚型、肿瘤侵袭性和低生存率相关。EMR2还通过产生活性氧(ROS)和脱颗粒来调节中性粒细胞的功能。已经研究了可能的治疗方法,例如通过下调EMR2基因或通过抗EMR2抗体刺激小胶质细胞和单核细胞来抑制肿瘤启动细胞。本文综述了EMR2受体的相关知识,为进一步研究EMR2受体在胶质瘤的临床进化和肿瘤生物学中的作用提供了动力,以期找到新的调节剂治疗方法。
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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