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多组学分析揭示调节氧化应激以促进口腔鳞状细胞癌进展的细胞间通讯。

Multi-omics analysis deciphers intercellular communication regulating oxidative stress to promote oral squamous cell carcinoma progression.

作者信息

Zhang Hongrong, Qian Yemei, Zhang Yang, Zhou Xue, Shen Shiying, Li Jingyi, Sun Zheyi, Wang Weihong

机构信息

Department of Oral and Maxillofacial Surgery, Affiliated Stomatology Hospital of Kunming Medical University, Kunming, China.

Yunnan Key Laboratory of Stomatology, Kunming, China.

出版信息

NPJ Precis Oncol. 2024 Nov 21;8(1):272. doi: 10.1038/s41698-024-00764-x.

DOI:10.1038/s41698-024-00764-x
PMID:39572698
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11582705/
Abstract

Oral squamous cell carcinoma (OSCC) is a common malignant tumor in the head and neck, associated with high recurrence and poor prognosis. We performed an integrated analysis of single-cell RNA and spatial transcriptomic data from cancerous and normal tissues to create a comprehensive atlas of epithelial cells and cancer-associated fibroblasts (CAFs). Our findings show that AKR1C3 epithelial cells, located at the tumor's stromal front, exhibit significant copy number variation and poor prognostic indicators, suggesting a role in tumor invasion. We also identified a distinct group of early-stage CAFs (named OSCC_Normal, characterized by ADH1B, MFAP4, and PLA2G2A) that interact with AKR1C3+ cells, where OSCC_Normal may inhibit the FOXO1 redox switch in these epithelial cells via the IGF1/IGF1R pathway, causing oxidative stress overload. Conversely, AKR1C3 cells use ITGA6/ITGB4 receptor to counteract the effects of OSCC_Normal, promoting cancer invasion. This study unveils complex interactions within the OSCC tumor microenvironment.

摘要

口腔鳞状细胞癌（OSCC）是头颈部常见的恶性肿瘤，具有高复发率和不良预后。我们对来自癌组织和正常组织的单细胞RNA和空间转录组数据进行了综合分析，以创建上皮细胞和癌症相关成纤维细胞（CAF）的综合图谱。我们的研究结果表明，位于肿瘤基质前沿的AKR1C3上皮细胞表现出显著的拷贝数变异和不良预后指标，提示其在肿瘤侵袭中发挥作用。我们还鉴定出一组独特的早期CAF（命名为OSCC_Normal，以ADH1B、MFAP4和PLA2G2A为特征），它们与AKR1C3+细胞相互作用，其中OSCC_Normal可能通过IGF1/IGF1R途径抑制这些上皮细胞中的FOXO1氧化还原开关，导致氧化应激过载。相反，AKR1C3细胞利用ITGA6/ITGB4受体抵消OSCC_Normal的作用，促进癌症侵袭。这项研究揭示了OSCC肿瘤微环境中的复杂相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4620/11582705/dc621e36e0e0/41698_2024_764_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4620/11582705/aa7ac8b3b571/41698_2024_764_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4620/11582705/316a08bca4f1/41698_2024_764_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4620/11582705/af787935dd66/41698_2024_764_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4620/11582705/cbeadbe1b915/41698_2024_764_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4620/11582705/3250edad34cc/41698_2024_764_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4620/11582705/dc621e36e0e0/41698_2024_764_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4620/11582705/aa7ac8b3b571/41698_2024_764_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4620/11582705/b6d780fc434f/41698_2024_764_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4620/11582705/9a04f39e54ba/41698_2024_764_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4620/11582705/316a08bca4f1/41698_2024_764_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4620/11582705/af787935dd66/41698_2024_764_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4620/11582705/cbeadbe1b915/41698_2024_764_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4620/11582705/3250edad34cc/41698_2024_764_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4620/11582705/dc621e36e0e0/41698_2024_764_Fig8_HTML.jpg

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