Department of Surgery, Fourth Affiliated Hospital, Hebei Medical University, Shijiazhuang, Hebei 050017, P.R. China.
Department of Stomatology, Second Hospital of Shijiazhuang, Shijiazhuang, Hebei 050000, P.R. China.
Oncol Rep. 2019 Feb;41(2):895-907. doi: 10.3892/or.2018.6870. Epub 2018 Nov 15.
Long non‑coding RNAs (lncRNAs) have been consistently demonstrated to be involved in oral squamous cell carcinoma (OSCC) as either tumor oncogenes or tumor suppressors. However, the underlying mechanisms of OSCC tumorigenesis and development have not yet been fully elucidated. The expression profiles of mRNAs and lncRNAs in OSCC were analyzed by a microarray assay. To verify the results of the microarray, 10 differentially expressed lncRNAs were randomly selected and measured by quantitative RT‑PCR (qRT‑PCR). Gene Ontology (GO) and metabolic pathway analyses were performed to analyze gene function and identify enriched pathways. Subsequently, two independent algorithms were used to predict the target genes of the lncRNAs. We identified 2,294 lncRNAs and 1,938 mRNAs that were differentially expressed in all three OSCC tissues by a microarray assay. Through the construction of co‑expression networks of differentially expressed genes, 4 critical lncRNAs nodes were identified as potential key factors in the pathogenesis of OSCC. Expression of the 4 critical lncRNA nodes was not associated with age, sex, smoking or tumor location (P>0.05) but was positively correlated with clinical stage, lymphatic metastasis, distant metastasis and survival status (P<0.05). Kaplan‑Meier analysis demonstrated that low expression levels of these 4 critical lncRNA nodes contributed to poor median progression‑free survival (PFS) and overall survival (OS) (P<0.05). GO and pathway analyses indicated that the functions and enriched pathways of many dysregulated genes are associated with cancer. Potential target genes of dysregulated lncRNAs were enriched in 43 metabolic pathways, with cancer pathways being the primary enrichment pathways. In summary, we analyzed the profile of lncRNAs in OSCC and identified the functions and enriched metabolic pathways of both dysregulated mRNAs and the target genes of dysregulated lncRNAs, providing new insights into molecular markers and therapeutic targets for OSCC.
长链非编码 RNA（lncRNA）已被证实参与口腔鳞状细胞癌（OSCC）的发生，其可作为肿瘤癌基因或肿瘤抑制因子。然而，OSCC 发生和发展的潜在机制尚未完全阐明。通过微阵列分析检测 OSCC 中 mRNA 和 lncRNA 的表达谱。为了验证微阵列的结果，随机选择了 10 个差异表达的 lncRNA 并通过实时定量 PCR（qRT-PCR）进行测量。进行基因本体论（GO）和代谢途径分析，以分析基因功能并确定富集途径。随后，使用两种独立的算法来预测 lncRNA 的靶基因。通过微阵列分析，我们在所有三种 OSCC 组织中鉴定出 2,294 个 lncRNA 和 1,938 个差异表达的 mRNA。通过差异表达基因的共表达网络构建，鉴定出 4 个关键 lncRNA 节点作为 OSCC 发病机制中的潜在关键因素。4 个关键 lncRNA 节点的表达与年龄、性别、吸烟或肿瘤位置无关（P>0.05），但与临床分期、淋巴转移、远处转移和生存状态呈正相关（P<0.05）。Kaplan-Meier 分析表明，这些 4 个关键 lncRNA 节点的低表达水平与较差的中位无进展生存期（PFS）和总生存期（OS）相关（P<0.05）。GO 和途径分析表明，许多失调基因的功能和富集途径与癌症相关。失调 lncRNA 的潜在靶基因在 43 个代谢途径中富集，其中癌症途径是主要的富集途径。综上所述，我们分析了 OSCC 中 lncRNA 的谱，并确定了失调 mRNA 和失调 lncRNA 的靶基因的功能和富集代谢途径，为 OSCC 的分子标志物和治疗靶点提供了新的见解。
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