Department of Otolaryngology Head and Neck Surgery, 303 Hospital of PLA Guangxi Zhuang Autonomous Region, Nanning, China.
Department of Cell Biology and Genetics, School of Pre-clinical Medicine, Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, China.
Pathol Res Pract. 2019 May;215(5):963-976. doi: 10.1016/j.prp.2019.02.002. Epub 2019 Feb 4.
The role of miR-99a-3p in Head and neck squamous cell carcinoma (HNSCC) has not been reported. Therefore, in this study, we examined the expression level and its molecular mechanisms of miR-99a-3p in HNSCC.
MiR-99a-3p-related miRNA-chip and miRNA-sequencing data were collected. We then carried out meta-analyses to pool the standard mean difference (SMD) value and generate a summarized receiver operating characteristic (sROC) curve. MiR-99a-3p mimic was transfected into FaDu cells and those genes influenced by miR-99a-3p were gathered. The target genes were also predicted from 12 tools through miRwalk2.0, and combined with differentially expressed genes in HNSCC from the The Cancer Genome Atlas and Genotype-Tissue Expression sequencing databases. FunRich and DAVID were used for the pathway signaling analyses for the potential targets of miR-99a-3p in HNSCC.
The SMD was -0.30 (95% CI: -0.51, -0.08) in the fixed-effect model and -0.28 (95% CI: -0.67, 0.10) in the random-effect model (I2 = 60%), indicating a reduced expression level of miR-99a-3p in HNSCC tissues based on 1167 cases. In the sROC curve, the area under the curve (AUC) was 0.77 (95% CI: 0.73, 0.81). The 251 potential targets of miR-99a-3p were enriched in several pathways related to cancer, with the "Pathways in cancer" standing at the top. vascular endothelial growth factor A was selected as an example with up-regulated trend in HNSCC tissues.
MiR-99a-3p exhibits a significant lower expression status in HNSCC, and this reduced or deletion status promotes the malignant progression of HNSCC. However, its molecular mechanism is still unclear and requires further investigation.
miR-99a-3p 在头颈部鳞状细胞癌（HNSCC）中的作用尚未报道。因此，在本研究中，我们检查了 miR-99a-3p 在 HNSCC 中的表达水平及其分子机制。
收集了 miR-99a-3p 相关的 miRNA 芯片和 miRNA 测序数据。然后，我们进行了荟萃分析，以汇总标准均数差（SMD）值并生成汇总受试者工作特征（sROC）曲线。将 miR-99a-3p 模拟物转染到 FaDu 细胞中，并收集受 miR-99a-3p 影响的基因。通过 miRwalk2.0 从 12 个工具预测靶基因，并与 The Cancer Genome Atlas 和 Genotype-Tissue Expression 测序数据库中 HNSCC 的差异表达基因相结合。使用 FunRich 和 DAVID 对 miR-99a-3p 在 HNSCC 中的潜在靶基因进行通路信号分析。
在固定效应模型中，SMD 为-0.30（95%CI：-0.51，-0.08），在随机效应模型中为-0.28（95%CI：-0.67，0.10）（I2=60%），表明基于 1167 例，HNSCC 组织中 miR-99a-3p 的表达水平降低。在 sROC 曲线中，曲线下面积（AUC）为 0.77（95%CI：0.73，0.81）。miR-99a-3p 的 251 个潜在靶基因富集在与癌症相关的几个通路中，其中“癌症通路”位居榜首。血管内皮生长因子 A 是 HNSCC 组织中上调趋势的一个例子。
miR-99a-3p 在 HNSCC 中表达水平显著降低，这种降低或缺失状态促进了 HNSCC 的恶性进展。然而，其分子机制尚不清楚，需要进一步研究。
