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基于高通量测序的舌癌转录组分析。

Transcriptome analysis of tongue cancer based on high‑throughput sequencing.

机构信息

Department of Head and Neck Surgery, Nantong Tumor Hospital, Nantong, Jiangsu 226361, P.R. China.

Department of Otorhinolaryngology Head and Neck Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu 226001, P.R. China.

出版信息

Oncol Rep. 2020 Jun;43(6):2004-2016. doi: 10.3892/or.2020.7560. Epub 2020 Mar 23.

Abstract

Tongue cancer is one of the most common types of cancer, but its molecular etiology and pathogenesis remain unclear. The aim of the present study was to elucidate the pathogenesis of tongue cancer and investigate novel potential diagnostic and therapeutic targets. Four matched pairs of tongue cancer and paracancerous tissues were collected for RNA sequencing (RNA‑Seq), and the differentially expressed genes were analyzed. The RNA‑Seq data of tongue cancer tissues were further analyzed using bioinformatics and reverse transcription‑quantitative PCR analysis. The sequenced reads were quantified and qualified in accordance with the analysis demands. The transcriptomes of the tongue cancer tissues and paired paracancerous tissues were analyzed, and 1,700 upregulated and 2,249 downregulated genes were identified. Gene Ontology analysis uncovered a significant enrichment in the terms associated with extracellular matrix (ECM) organization, cell adhesion and collagen catabolic processes. Kyoto Encyclopedia of Genes and Genomes analysis demonstrated that these differentially expressed genes were mainly enriched in the focal adhesion pathway, ECM‑receptor interaction pathway, phosphoinositide 3‑kinase (PI3K)‑Akt pathway, and cell adhesion molecules. Comprehensive analyses of the gene tree and pathway network revealed that the majority of cell cycle genes were upregulated, while the majority of the genes associated with intracellular response, cell adhesion and cell differentiation were downregulated. The ECM‑receptor interaction, focal adhesion kinase (FAK) and PI3K‑Akt pathways were closely associated with one another and held key positions in differential signaling pathways. The ECM‑receptor, FAK and PI3K‑Akt signaling pathways were found to synergistically promote tongue cancer occurrence and progression, and may serve as potential diagnostic and therapeutic targets for this type of cancer.

摘要

舌癌是最常见的癌症类型之一,但它的分子病因和发病机制仍不清楚。本研究旨在阐明舌癌的发病机制,并研究新的潜在诊断和治疗靶点。收集了四对匹配的舌癌和癌旁组织进行 RNA 测序(RNA-seq),并分析了差异表达的基因。进一步对舌癌组织的 RNA-seq 数据进行了生物信息学分析和逆转录定量 PCR 分析。根据分析需求对测序reads 进行定量和质量评估。分析了舌癌组织和配对癌旁组织的转录组,鉴定出 1700 个上调基因和 2249 个下调基因。GO 分析显示,这些基因显著富集在与细胞外基质(ECM)组织、细胞黏附和胶原代谢过程相关的术语中。京都基因与基因组百科全书(KEGG)分析表明,这些差异表达基因主要富集在粘着斑、ECM-受体相互作用、PI3K-Akt 信号通路和细胞黏附分子信号通路中。基因树和通路网络的综合分析表明,大多数细胞周期基因上调,而与细胞内反应、细胞黏附和细胞分化相关的大多数基因下调。ECM-受体相互作用、粘着斑激酶(FAK)和 PI3K-Akt 信号通路密切相关,在差异信号通路中处于关键位置。ECM-受体、FAK 和 PI3K-Akt 信号通路协同促进舌癌的发生和发展,可能成为这种癌症的潜在诊断和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3b6/7160550/9e819adf865e/OR-43-06-2004-g00.jpg

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