Laboratory of Gastrointestinal Onco-Pathology, Cancer Institute, The First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning Province, China.
Biomed Res Int. 2020 May 13;2020:6726759. doi: 10.1155/2020/6726759. eCollection 2020.
The AT-hook transcription factor, AKNA, is a nuclear protein that affects a few physiological and pathological processes including cancer. Here, we investigated the role of in gastric cancer (GC). By using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot assays, was found deregulated in both GC cell lines and 32 paired GC tissues. Subsequently, Kaplan-Meier analysis and clinicopathological analysis were conducted using both 32 GC cases' data above and RNA-Seq data of in 354 GC patients and the corresponding clinical-pathological data obtained from The Cancer Genome Atlas (TCGA), and expression was found closely related to location, metastasis, and TNM staging of GC. Then, the potential molecular mechanisms of in GC were explored by gene set enrichment analysis (GSEA), qRT-PCR, and Western blot assays. was found to be a hub gene related to homotypic cell to cell adhesion, regulation of cell to cell adhesion, leukocyte cell to cell adhesion, and regulation of T cell proliferation in GC. GO analysis revealed that involved in the regulation of epithelial-mesenchymal transition (EMT)-related pathways including chemokine signaling pathway, cytokine to cytokine receptor interaction, cell adhesion molecules, and jak-stat signaling pathway in GC. To explore the regulation of expression, and were used to predict the possible miRNA which targeted and found the expression of was negatively correlated to miR-762 which could be sponged by circTRNC18. In conclusion, could function as a tumor suppressor by modulating EMT-related pathways in GC. The expression of might be regulated by circTRNC18/miR-762 axis. could serve as a potential biomarker and an effective target for GC diagnosis and therapy.
AT 钩转录因子 AKNA 是一种核蛋白，可影响包括癌症在内的一些生理和病理过程。在这里，我们研究了在胃癌（GC）中的作用。通过使用定量实时聚合酶链反应（qRT-PCR）和 Western blot 分析，在 GC 细胞系和 32 对 GC 组织中发现失调。随后，使用上述 32 个 GC 病例的数据和 RNA-Seq 数据对 354 个 GC 患者中的进行 Kaplan-Meier 分析和临床病理分析，以及从癌症基因组图谱（TCGA）获得的相应临床病理数据，发现表达与 GC 的位置、转移和 TNM 分期密切相关。然后，通过基因集富集分析（GSEA）、qRT-PCR 和 Western blot 分析探索在 GC 中的潜在分子机制。发现是与同质细胞间粘附、细胞间粘附调节、白细胞细胞间粘附和 GC 中 T 细胞增殖调节相关的基因。GO 分析表明，涉及上皮-间充质转化（EMT）相关途径的调节，包括趋化因子信号通路、细胞因子-细胞因子受体相互作用、细胞粘附分子和 jak-stat 信号通路在 GC 中。为了探索表达的调节，使用和预测可能靶向的 miRNA，并发现的表达与 miR-762 呈负相关，miR-762 可被 circTRNC18 海绵化。总之，可通过调节 GC 中的 EMT 相关途径发挥肿瘤抑制因子的作用。的表达可能受 circTRNC18/miR-762 轴的调节。可作为 GC 诊断和治疗的潜在生物标志物和有效靶点。
