Tong Wangxia, Yang Lilan, Liu Li, Liu Xudong, Luo Ning
The Medical Department of Hepatology, Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine, Nanning, 530011, People's Republic of China.
RuiKang Hospital Affiliated to Guangxi University of Chinese Medicine, Nanning, 530011, People's Republic of China.
Onco Targets Ther. 2022 May 18;15:555-570. doi: 10.2147/OTT.S348843. eCollection 2022.
As a novel genetic biomarker, little information is available about the possible role of in different malignant tumors and in hepatocellular carcinoma (HCC).
Based on The Cancer Genome Atlas (TCGA) database, the expression level of in pan-cancer and hepatocellular carcinoma samples was first determined using bioinformatics analysis. The potential relationship between the expression level as well as the clinical characteristics and the molecular mechanisms through which can promote the proliferation, invasion and migration of HCC cells was evaluated. In addition, cell-based studies and in vivo experiments were used to verify the bioinformatics analysis results.
Bioinformatics analysis showed that expression was significantly increased in 18 human malignancies and the gene expression level was positively correlated with poor clinical prognosis in kidney renal papillary cell carcinoma (KIRP), pheochromocytoma and paraganglioma (PCPG) and liver hepatocellular carcinoma (LIHC). The main type of genetic variation of was amplification, and the increase of mRNA expression level was directly related to the amplification of this gene. The expression level of in patients with primary HCC was positively correlated with poor clinical prognosis, as well as the clinical grade and stage of carcinoma. Gene set enrichment analysis (GSEA) analysis showed that high expression of could activate Wnt/β-catenin signaling pathway. Moreover, in vitro and in vivo experiments showed that gene silencing significantly inhibited the proliferation, migration and invasion of Huh7 and SK-HEP-1 cells and decreased the expression of SPIN1, Wnt1, β-catenin and cyclin D1 but increased the expression of AXIN2.
is highly expressed in pan-cancer and HCC samples. This factor can effectively promote the invasion and migration of hepatocellular carcinoma (HCC) cells by activating Wnt/β-catenin signaling pathway, and thus can serve as a potential therapeutic target for HCC management.
作为一种新型的遗传生物标志物，关于其在不同恶性肿瘤及肝细胞癌（HCC）中的可能作用，目前所知甚少。
基于癌症基因组图谱（TCGA）数据库，首先通过生物信息学分析确定其在泛癌和肝细胞癌样本中的表达水平。评估该表达水平与临床特征之间的潜在关系，以及其促进HCC细胞增殖、侵袭和迁移的分子机制。此外，通过细胞实验和体内实验验证生物信息学分析结果。
生物信息学分析显示，在18种人类恶性肿瘤中该表达显著增加，且基因表达水平与肾肾乳头状细胞癌（KIRP）、嗜铬细胞瘤和副神经节瘤（PCPG）以及肝肝细胞癌（LIHC）的不良临床预后呈正相关。该基因的主要遗传变异类型为扩增，其mRNA表达水平的增加与该基因的扩增直接相关。原发性HCC患者中该表达水平与不良临床预后以及癌的临床分级和分期呈正相关。基因集富集分析（GSEA）表明，该基因的高表达可激活Wnt/β-连环蛋白信号通路。此外，体外和体内实验表明，该基因沉默可显著抑制Huh7和SK-HEP-1细胞的增殖、迁移和侵袭，并降低SPIN1、Wnt1、β-连环蛋白和细胞周期蛋白D1的表达，但增加AXIN2的表达。
在泛癌和HCC样本中高表达。该因子可通过激活Wnt/β-连环蛋白信号通路有效促进肝细胞癌（HCC）细胞的侵袭和迁移，因此可作为HCC治疗的潜在靶点。
