微RNA在胃癌肿瘤微环境中的作用

IF 27.7 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Molecular Cancer Pub Date : 2024-08-20 DOI:10.1186/s12943-024-02084-x
Xianzhe Yu, Yin Zhang, Fengming Luo, Qinghua Zhou, Lingling Zhu
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引用次数: 0

摘要

胃癌(GC)是发病机制不明的最致命恶性肿瘤之一。由于其耐药性、高复发率以及缺乏可靠的早期检测技术,大多数患者预后不良。因此,确定新的肿瘤生物标志物和治疗靶点至关重要。本综述旨在通过总结微小RNA(miRNA)调控肿瘤微环境(TME)的过程并强调其在TME中的关键作用,为改善GC患者的预后提供新的见解。通过重点研究 GC TME 中肿瘤细胞、细胞外基质、血管、癌症相关成纤维细胞和免疫细胞之间的相互作用,我们进行了全面的文献综述。研究还特别探讨了被称为 miRNA 的非编码 RNA 在通过各种信号通路、细胞因子、生长因子和外泌体调节 TME 方面的作用。在 GC 中,肿瘤的形成、转移和治疗受到 TME 内相互作用的显著影响。miRNA 通过多种信号通路、细胞因子、生长因子和外泌体调节这些相互作用,从而调控肿瘤的进展。miRNAs 的失调会影响细胞增殖、分化、血管生成、转移和耐药性等关键细胞过程,从而导致 GC 的发病机制。通过了解 miRNAs 控制 TME 的机制,可以确定潜在的生物标志物和治疗靶点,从而改善 GC 患者的预后。
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The role of microRNAs in the gastric cancer tumor microenvironment
Gastric cancer (GC) is one of the deadliest malignant tumors with unknown pathogenesis. Due to its treatment resistance, high recurrence rate, and lack of reliable early detection techniques, a majority of patients have a poor prognosis. Therefore, identifying new tumor biomarkers and therapeutic targets is essential. This review aims to provide fresh insights into enhancing the prognosis of patients with GC by summarizing the processes through which microRNAs (miRNAs) regulate the tumor microenvironment (TME) and highlighting their critical role in the TME. A comprehensive literature review was conducted by focusing on the interactions among tumor cells, extracellular matrix, blood vessels, cancer-associated fibroblasts, and immune cells within the GC TME. The role of noncoding RNAs, known as miRNAs, in modulating the TME through various signaling pathways, cytokines, growth factors, and exosomes was specifically examined. Tumor formation, metastasis, and therapy in GC are significantly influenced by interactions within the TME. miRNAs regulate tumor progression by modulating these interactions through multiple signaling pathways, cytokines, growth factors, and exosomes. Dysregulation of miRNAs affects critical cellular processes such as cell proliferation, differentiation, angiogenesis, metastasis, and treatment resistance, contributing to the pathogenesis of GC. miRNAs play a crucial role in the regulation of the GC TME, influencing tumor progression and patient prognosis. By understanding the mechanisms through which miRNAs control the TME, potential biomarkers and therapeutic targets can be identified to improve the prognosis of patients with GC.
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来源期刊
Molecular Cancer
Molecular Cancer 医学-生化与分子生物学
CiteScore
54.90
自引率
2.70%
发文量
224
审稿时长
2 months
期刊介绍: Molecular Cancer is a platform that encourages the exchange of ideas and discoveries in the field of cancer research, particularly focusing on the molecular aspects. Our goal is to facilitate discussions and provide insights into various areas of cancer and related biomedical science. We welcome articles from basic, translational, and clinical research that contribute to the advancement of understanding, prevention, diagnosis, and treatment of cancer. The scope of topics covered in Molecular Cancer is diverse and inclusive. These include, but are not limited to, cell and tumor biology, angiogenesis, utilizing animal models, understanding metastasis, exploring cancer antigens and the immune response, investigating cellular signaling and molecular biology, examining epidemiology, genetic and molecular profiling of cancer, identifying molecular targets, studying cancer stem cells, exploring DNA damage and repair mechanisms, analyzing cell cycle regulation, investigating apoptosis, exploring molecular virology, and evaluating vaccine and antibody-based cancer therapies. Molecular Cancer serves as an important platform for sharing exciting discoveries in cancer-related research. It offers an unparalleled opportunity to communicate information to both specialists and the general public. The online presence of Molecular Cancer enables immediate publication of accepted articles and facilitates the presentation of large datasets and supplementary information. This ensures that new research is efficiently and rapidly disseminated to the scientific community.
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