Ahmed Hussein Zwamel, Abdulrahman T Ahmad, Farag M A Altalbawy, H Malathi, Amandeep Singh, Majid S Jabir, Zafar Aminov, Madan Lal, Abhinav Kumar, Sabrean F Jawad
{"title":"外泌体rna和EZH2:揭示驱动肿瘤进展的分子对话。","authors":"Ahmed Hussein Zwamel, Abdulrahman T Ahmad, Farag M A Altalbawy, H Malathi, Amandeep Singh, Majid S Jabir, Zafar Aminov, Madan Lal, Abhinav Kumar, Sabrean F Jawad","doi":"10.1007/s12032-025-02648-x","DOIUrl":null,"url":null,"abstract":"<p><p>The EZH2 gene encodes an enzyme that is part of the epigenetic factor Polycomb Repressive Complex 2 (PRC2). In order to control gene expression, PRC2 mainly modifies chromatin structure. In this complex process, EZH2 methylates histone proteins, which in turn suppresses further RNA transcriptions. As a result, EZH2 dysregulations can occasionally induce abnormal gene expression patterns, which can aid in the development and progression of cancer. Non-coding RNAs significantly impact the expression of EZH2 through epigenetic mechanisms. Meanwhile, normal and cancerous cells frequently release vesicles into the extracellular matrix, also known as exosomes, that occasionally carry RNA molecules from their origin cells, including messenger RNAs, microRNAs, and other non-coding RNAs. Thus exosomes are granted the ability to regulate numerous physiological functions and act as crucial messengers between cells by influencing gene expression in the recipient cell. We conducted this review to focus on EZH2's substantial biological role and the mechanisms that regulate it, driven by the desire to understand the possible impact of exosomal RNAs on EZH2 expression.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"103"},"PeriodicalIF":2.8000,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Exosomal RNAs and EZH2: unraveling the molecular dialogue driving tumor progression.\",\"authors\":\"Ahmed Hussein Zwamel, Abdulrahman T Ahmad, Farag M A Altalbawy, H Malathi, Amandeep Singh, Majid S Jabir, Zafar Aminov, Madan Lal, Abhinav Kumar, Sabrean F Jawad\",\"doi\":\"10.1007/s12032-025-02648-x\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The EZH2 gene encodes an enzyme that is part of the epigenetic factor Polycomb Repressive Complex 2 (PRC2). In order to control gene expression, PRC2 mainly modifies chromatin structure. In this complex process, EZH2 methylates histone proteins, which in turn suppresses further RNA transcriptions. As a result, EZH2 dysregulations can occasionally induce abnormal gene expression patterns, which can aid in the development and progression of cancer. Non-coding RNAs significantly impact the expression of EZH2 through epigenetic mechanisms. Meanwhile, normal and cancerous cells frequently release vesicles into the extracellular matrix, also known as exosomes, that occasionally carry RNA molecules from their origin cells, including messenger RNAs, microRNAs, and other non-coding RNAs. Thus exosomes are granted the ability to regulate numerous physiological functions and act as crucial messengers between cells by influencing gene expression in the recipient cell. We conducted this review to focus on EZH2's substantial biological role and the mechanisms that regulate it, driven by the desire to understand the possible impact of exosomal RNAs on EZH2 expression.</p>\",\"PeriodicalId\":18433,\"journal\":{\"name\":\"Medical Oncology\",\"volume\":\"42 4\",\"pages\":\"103\"},\"PeriodicalIF\":2.8000,\"publicationDate\":\"2025-03-12\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Medical Oncology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1007/s12032-025-02648-x\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Medical Oncology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s12032-025-02648-x","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ONCOLOGY","Score":null,"Total":0}
Exosomal RNAs and EZH2: unraveling the molecular dialogue driving tumor progression.
The EZH2 gene encodes an enzyme that is part of the epigenetic factor Polycomb Repressive Complex 2 (PRC2). In order to control gene expression, PRC2 mainly modifies chromatin structure. In this complex process, EZH2 methylates histone proteins, which in turn suppresses further RNA transcriptions. As a result, EZH2 dysregulations can occasionally induce abnormal gene expression patterns, which can aid in the development and progression of cancer. Non-coding RNAs significantly impact the expression of EZH2 through epigenetic mechanisms. Meanwhile, normal and cancerous cells frequently release vesicles into the extracellular matrix, also known as exosomes, that occasionally carry RNA molecules from their origin cells, including messenger RNAs, microRNAs, and other non-coding RNAs. Thus exosomes are granted the ability to regulate numerous physiological functions and act as crucial messengers between cells by influencing gene expression in the recipient cell. We conducted this review to focus on EZH2's substantial biological role and the mechanisms that regulate it, driven by the desire to understand the possible impact of exosomal RNAs on EZH2 expression.
期刊介绍:
Medical Oncology (MO) communicates the results of clinical and experimental research in oncology and hematology, particularly experimental therapeutics within the fields of immunotherapy and chemotherapy. It also provides state-of-the-art reviews on clinical and experimental therapies. Topics covered include immunobiology, pathogenesis, and treatment of malignant tumors.