肿瘤微环境的作用和靶向治疗策略
商务英语专业课程Tumor Microenvironment: Its Role and Targeted Therapeutic Strategies
成都来福士摘要
肿瘤微环境是肿瘤生长和发展中具有重要作用的因素。它包括肿瘤细胞、细胞外基质、免疫细胞、血管、神经元及其释放的信号分子等多个组成部分，并与肿瘤细胞之间相互作用。肿瘤微环境的变化会影响肿瘤生长、进展及对治疗的应答，因此针对肿瘤微环境的靶向治疗策略逐渐成为当前肿瘤治疗研究的热点。本文综述了肿瘤微环境的主要组成成分及其相互作用，探讨了靶向干扰肿瘤微环境的治疗策略。
关键词：肿瘤微环境；靶向治疗；组成成分；治疗策略
Tumor Microenvironment: Its Role and Targeted Therapeutic Strategies
Abstract
Tumor microenvironment plays a crucial role in tumor growth and development. It compri
s various components, including tumor cells, extracellular matrix, immune cells, blood vesls, neurons, and signaling molecules relead by the components, all of which interact with tumor cells. Changes in the tumor microenvironment can affect tumor growth, progression, and respon to therapy, making targeted therapeutic strategies against the tumor microenvironment a current hot spot in tumor rearch. This review summarizes the main components of the tumor microenvironment and their interactions, and discuss therapeutic strategies targeted at interfering with the tumor microenvironment.
Keywords: tumor microenvironment; targeted therapy; components; therapeutic strategies
Introduction
Tumor microenvironment (TME) refers to the complex and dynamic environment in which tumor cells grow and develop. It consists of tumor cells, extracellular matrix (ECM), immune cells, blood vesls, neurons, and signaling molecules relead by the compoecosystem
nents, among others (1). TME is an esntial regulator of tumor growth, metastasis, and patient outcomes, and its components interact with tumor cells in complex and dynamic ways, sometimes promoting and sometimes suppressing tumor growth (2). Therefore, understanding TME and its role in tumor growth and development is critical for the design of effective cancer therapies.
benchmark什么意思Components of TME汤唯英语
Tumor cells: The tumor cells themlves are a part of TME, and their nature, number, and behavior can affect the entire microenvironment. Tumor cells crete various factors that regulate tumor cell proliferation, migration, and invasion, and also signal the recruitment of other components of the microenvironment (3).
ECM: ECM is a network of proteins, peptides, and carbohydrates that forms the physical scaffold of tissues and organs. ECM in TME differs significantly from that in normal tissues and plays a vital role in regulating cell behavior. Changes in ECM can increa tumor cell proliferation, motility, and survival (4).
Immune cells: Immune cells, such as T lymphocytes, B lymphocytes, natural killer (NK) cells, and myeloid-derived suppressor cells (MDSCs), play a significant role in TME. Immune cells are involved in both tumor initiation and progression, and their role is dependent on their activation status, location, and type (5).
Blood vesls: New blood vesl formation is necessary for tumor growth and survival, and angiogenesis is one of the mechanisms by which TME regulates tumor growth. Endothelial cells, which make up blood vesls, help support tumor growth and survival through various mechanisms (6).
Neurons: Neurotransmitters and neuropeptides relead by neurons in the tumor microenvironment can have both pro- and anti-tumor effects, depending on the microenvironment and tumor context (7).
好听的法文歌曲Signaling molecules: Various signaling molecules are relead by the different components of TME and modulate the growth and behavior of tumor cells. The molecules include cytokines, chemokines, growth factors, and extracellular vesicles (8).
Interactions in TME
TME components interact in complex ways, and the interactions can be circuitous, reinforcing, or antagonistic. For example, cancer-associated fibroblasts (CAFs), which are stromal cells in TME, interact with immune cells and tumor cells to promote tumor growth and progression (9). CAFs produce ECM proteins that increa tumor cell proliferation, migration, and invasiveness. They also crete cytokines and chemokines that recruit other TME components, including immune cells. Tumor cells can also interact with immune cells in TME to avoid immune surveillance and induce immune tolerance. For example, tumor cells express programmed death-ligand 1 (PD-L1), which can bind to programmed death-1 (PD-1) on activated T cells and inhibit T-cell activity (10).
administrative
Targeted Therapeutic Strategies
quGiven the complexity of TME, targeted therapeutic strategies hold immen promi in cancer treatment. Many approaches are being explored to interfere with TME, including inhibition of angiogenesis, immunomodulation, ECM remodeling, and modulation of signa
ling pathways (11). For example, antiangiogenic agents targeting vascular endothelial growth factor (VEGF) and its receptor VEGFR have shown promi in inhibiting new blood vesl formation in TME (12). Immunomodulatory agents targeting immune checkpoints, such as PD-L1 and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), have shown remarkable respons in certain cancers, such as melanoma and non-small cell lung cancer (13). ECM-modulating agents, such as lysyl oxida-like 2 (LOXL2) inhibitors, have shown promi in preventing ECM remodeling in TME (14). Modulation of signaling pathways involved in TME, such as tho mediated by transforming growth factor-beta (TGF-β) or hypoxia-inducible factor 1-alpha (HIF-1α), also holds promi (15).
