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口腔鳞状细胞癌中的肿瘤微环境

Tumor microenvironment in oral squamous cell carcinoma.

作者信息

Li Chenxi, Dong Xiaodan, Li Bo

机构信息

Department of Oral Anatomy and Physiology, Jilin Provincial Key Laboratory of Oral Biomedical Engineering, Hospital of Stomatology, Jilin University, Changchun, China.

出版信息

Front Immunol. 2024 Dec 18;15:1485174. doi: 10.3389/fimmu.2024.1485174. eCollection 2024.


DOI:10.3389/fimmu.2024.1485174
PMID:39744628
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11688467/
Abstract

Oral squamous cell carcinoma (OSCC) is a highly aggressive and malignant tumor of oral cavity with a poor prognosis and high mortality due to the limitations of existing therapies. The significant role of tumor microenvironment (TME) in the initiation, development, and progression of OSCC has been widely recognized. Various cells in TME, including tumor-associated macrophages (TAMs), cancer-associated fibroblasts (CAFs), T lymphocytes, tumor-associated neutrophils (TANs), myeloid-derived suppressor cells (MDSCs) and dendritic cells (DCs), form a complicated and important cellular network to modulate OSCC proliferation, invasion, migration, and angiogenesis by secreting RNAs, proteins, cytokines, and metabolites. Understanding the interactions among cells in TME provides the foundation for advanced clinical diagnosis and therapies. This review summarizes the current literature that describes the role of various cellular components and other TME factors in the progression of OSCC, hoping to provide new ideas for the novel OSCC treatment strategies targeting the complicated cellular network and factors that mediate the interactive loops among cells in TME.

摘要

口腔鳞状细胞癌(OSCC)是一种侵袭性很强的口腔恶性肿瘤,由于现有治疗方法的局限性,其预后较差,死亡率较高。肿瘤微环境(TME)在OSCC的发生、发展和进展中的重要作用已得到广泛认可。TME中的各种细胞,包括肿瘤相关巨噬细胞(TAM)、癌症相关成纤维细胞(CAF)、T淋巴细胞、肿瘤相关中性粒细胞(TAN)、髓源性抑制细胞(MDSC)和树突状细胞(DC),形成了一个复杂而重要的细胞网络,通过分泌RNA、蛋白质、细胞因子和代谢产物来调节OSCC的增殖、侵袭、迁移和血管生成。了解TME中细胞间的相互作用为先进的临床诊断和治疗提供了基础。本综述总结了当前描述各种细胞成分和其他TME因素在OSCC进展中作用的文献,希望为针对复杂细胞网络和介导TME中细胞间相互作用环的因素的新型OSCC治疗策略提供新思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37e/11688467/fb80c4babc03/fimmu-15-1485174-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37e/11688467/5cf90454b778/fimmu-15-1485174-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37e/11688467/f53ce86c7f47/fimmu-15-1485174-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37e/11688467/0aff6df35219/fimmu-15-1485174-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37e/11688467/fb80c4babc03/fimmu-15-1485174-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37e/11688467/5cf90454b778/fimmu-15-1485174-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37e/11688467/f53ce86c7f47/fimmu-15-1485174-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37e/11688467/0aff6df35219/fimmu-15-1485174-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f37e/11688467/fb80c4babc03/fimmu-15-1485174-g004.jpg

相似文献

[1]
Tumor microenvironment in oral squamous cell carcinoma.

Front Immunol. 2024-12-18

[2]
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[3]
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[4]
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[5]
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[6]
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Am J Pathol. 2020-2-5

[7]
Cancer-associated fibroblasts promote oral squamous cell carcinoma progression through LOX-mediated matrix stiffness.

J Transl Med. 2021-12-20

[8]
Tumor-associated macrophages drive heterogenetic CD10 cancer stem cells to implement tumor-associated neutrophils reprogramming in oral squamous cell carcinoma.

Int J Biol Sci. 2025-1-13

[9]
The Role of Sonic Hedgehog Signaling in the Tumor Microenvironment of Oral Squamous Cell Carcinoma.

Int J Mol Sci. 2019-11-17

[10]
Exosomal miR-146b-5p derived from cancer-associated fibroblasts promotes progression of oral squamous cell carcinoma by downregulating HIPK3.

Cell Signal. 2023-6

引用本文的文献

[1]
Unravelling molecular mechanism of oral squamous cell carcinoma and genetic landscape: an insight into disease complexity, available therapies, and future considerations.

Front Immunol. 2025-8-13

[2]
Dysregulated PI3K/AKT signaling in oral squamous cell carcinoma: The tumor microenvironment and epigenetic modifiers as key drivers.

Oncol Res. 2025-7-18

[3]
Overlapping genes connect rheumatoid arthritis and head and neck cancer: coincidence or shared immune pathophysiology?

Front Med (Lausanne). 2025-6-18

[4]
Multiplex immunofluorescence assessment of macrophages and IL-23R in inflammatory and malignant diseases of the oral mucosa: a pilot study.

Front Immunol. 2025-4-14

本文引用的文献

[1]
Nanomedicines Targeting Tumor Cells or Tumor-Associated Macrophages for Combinatorial Cancer Photodynamic Therapy and Immunotherapy: Strategies and Influencing Factors.

Int J Nanomedicine. 2024

[2]
LncRNAPVT1 is Associated with Cancer-Associated Fibroblasts Proliferation Through Regulating TGF-βin Oral Squamous Cell Carcinoma.

Immunol Invest. 2024-11

[3]
Hsa_circRNA_101036 aggravates hypoxic-induced endoplasmic reticulum stress via the miR-21-3p/TMTC1 axis in oral squamous cell carcinoma.

Heliyon. 2024-6-13

[4]
Evaluation of Cytotoxic T Lymphocytes and Natural Killer Cell Distribution in Oral Squamous Cell Carcinoma and Oral Epithelial Dysplasia: An Immunohistochemical Study.

Cureus. 2024-3-17

[5]
Increased V-ATPase activity can lead to chemo-resistance in oral squamous cell carcinoma via autophagy induction: new insights.

Med Oncol. 2024-4-9

[6]
Spatial transcriptomics reveals that metabolic characteristics define the tumor immunosuppression microenvironment via iCAF transformation in oral squamous cell carcinoma.

Int J Oral Sci. 2024-1-30

[7]
Cancer-Associated Fibroblast Heterogeneity in Malignancy with Focus on Oral Squamous Cell Carcinoma.

Int J Mol Sci. 2024-1-21

[8]
ALDH3A1 upregulation inhibits neutrophils N2 polarization and halts oral cancer growth.

Oral Dis. 2024-10

[9]
PDGF-BB accelerates TSCC via fibroblast lactates limiting miR-26a-5p and boosting mitophagy.

Cancer Cell Int. 2024-1-2

[10]
Expansion of CD4+ cytotoxic T lymphocytes with specific gene expression patterns may contribute to suppression of tumor immunity in oral squamous cell carcinoma: single-cell analysis and experiments.

Front Immunol. 2023

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