EMP3: A promising biomarker for tumor prognosis and targeted cancer therapy

被引:1
|
作者
Zhu, Wenjing [1 ]
Song, Shu [2 ]
Xu, Yangchun [1 ]
Sheng, Hanyue [1 ]
Wang, Shuang [1 ]
机构
[1] Second Hosp Jilin Univ, Dept Dermatol, 218 Ziqiang St, Changchun 130041, Jilin, Peoples R China
[2] Univ Ottawa, Fac Med, Dept Biochem Microbiol & Immunol, Ottawa, ON, Canada
关键词
Epithelial membrane protein 3; cancer; transmembrane protein; signaling pathway; glioma; MEMBRANE-PROTEIN; 3; N-MYRISTOYLTRANSFERASE; CELL-PROLIFERATION; PANCREATIC-CANCER; SUPPRESSOR GENE; KINASE-C; EXPRESSION; CARCINOMA; MICROARRAY; SURVIVAL;
D O I
10.3233/CBM-230504
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Epithelial membrane protein 3 (EMP3) belongs to the peripheral myelin protein 22 kDa (PMP22) gene family, characterized by four transmembrane domains and widespread expression across various human tissues and organs. Other members of the PMP22 family, including EMP1, EMP2, and PMP22, have been linked to various cancers, such as glioblastoma, laryngeal cancer, nasopharyngeal cancer, gastric cancer, breast cancer, and endometrial cancer. However, few studies report on the function and relevance of EMP3 in tumorigenicity. Given the significant structural similarities among members of the PMP22 family, there are likely potential functional similarities as well. Previous studies have established the regulatory role of EMP3 in immune cells like T cells and macrophages. Additionally, EMP3 is found to be involved in critical signaling pathways, including HER2/PI3K/Akt, MAPK/ERK, and TGF-beta/Smad. Furthermore, EMP3 is associated with cell cycle regulation, cellular proliferation, and apoptosis. Hence, it is likely that EMP3 participates in cancer development through these aforementioned pathways and mechanisms. This review aims to systematically examine and summarize the structure and function of EMP3 and its association to various cancers. EMP3 is expected to emerge as a significant biological marker for tumor prognosis and a potential target in cancer therapeutics.
引用
收藏
页码:227 / 239
页数:13
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