Yuan Han-Mei, Pu Xiao-Feng, Wu Hui, Wu Chao
Department of Laboratory Medicine, The Eighth Affiliated Hospital, Sun Yat-sen University, Shenzhen 518033, Guangdong Province, China.
Department of Clinical Laboratory, The General Hospital of Western Theater Command, Chengdu 610000, Sichuan Province, China.
World J Gastrointest Oncol. 2023 Jul 15;15(7):1182-1199. doi: 10.4251/wjgo.v15.i7.1182.
Gastric cancer (GC) is a malignant tumor with high morbidity and mortality. Expression of is significantly elevated in GC. Abnormal expression of noncoding RNAs (ncRNAs) have been found in GC, including microRNA (miRNA) and long noncoding RNA (lncRNA). Competing endogenous RNA network plays an important regulatory role in GC. However, its specific regulatory mechanism has not been elucidated.
To gain insight into the ncRNA regulatory mechanism and immune microenvironment related to in GC.
RNA sequencing data and clinical information from The Cancer Genome Atlas data portal were used to analyze the expressions of , miRNA and lncRNA related to the prognosis of GC. Cox regression analysis and Kyoto Encyclopedia of Genes and Genomes analysis were performed to assess the risk factors and relevant function of . StarBase was used to predict the interaction of miRNA-lncRNA or miRNA-mRNA in GC. The relationship between , miR-144-3p and ENTPD1-AS1 were verified by dual luciferase reporter assay. The association of with immune cell infiltration were analyzed using the Tumor Immune Estimation Resource database and single sample gene set enrichment analysis. The expression of and macrophages in paired GC tissues were detected by immunohistochemical staining.
We verified that the upregulation of expression was associated with the prognosis of GC and was an independent risk factor for GC. miR-144-3p was downregulated and correlated with the prognosis of GC. miR-144-3p regulated the expression of through direct interaction with . ENTPD1-AS1 was elevated in GC and competitively bound to miR-144-3p, thus inhibiting the expression of miR-144-3p. ENTPD1-AS1 enhanced the expression of through sponging miR-144-3p. Compared to paired normal tissue, expression was upregulated at the protein level, especially in the middle and late stages of GC. The high expression of was positively linked to macrophage infiltration in GC.
regulated by ENTPD1-AS1-miR-144-3p was associated with poor prognosis and macrophage infiltration in GC. This could be a new biomarker and therapeutic target in GC.
胃癌（GC）是一种发病率和死亡率都很高的恶性肿瘤。[具体基因名称]在GC中的表达显著升高。在GC中已发现非编码RNA（ncRNA）表达异常，包括微小RNA（miRNA）和长链非编码RNA（lncRNA）。竞争性内源RNA网络在GC中起重要调节作用。然而，其具体调节机制尚未阐明。
深入了解GC中与[具体基因名称]相关的ncRNA调节机制和免疫微环境。
利用来自癌症基因组图谱数据门户的RNA测序数据和临床信息，分析与GC预后相关的[具体基因名称]、miRNA和lncRNA的表达。进行Cox回归分析和京都基因与基因组百科全书分析，以评估[具体基因名称]的危险因素和相关功能。利用StarBase预测GC中miRNA-lncRNA或miRNA-mRNA的相互作用。通过双荧光素酶报告基因检测验证[具体基因名称]、miR-144-3p和ENTPD1-AS1之间的关系。使用肿瘤免疫估计资源数据库和单样本基因集富集分析来分析[具体基因名称]与免疫细胞浸润的关联。通过免疫组织化学染色检测配对GC组织中[具体基因名称]和巨噬细胞的表达。
我们验证了[具体基因名称]表达上调与GC预后相关，并且是GC的独立危险因素。miR-144-3p表达下调且与GC预后相关。miR-144-3p通过与[具体基因名称]直接相互作用来调节其表达。ENTPD1-AS1在GC中升高，并与miR-144-3p竞争性结合，从而抑制miR-144-3p的表达。ENTPD1-AS1通过吸附miR-144-3p增强[具体基因名称]的表达。与配对的正常组织相比，[具体基因名称]在蛋白水平上表达上调，尤其是在GC的中晚期。[具体基因名称]的高表达与GC中的巨噬细胞浸润呈正相关。
ENTPD1-AS1-miR-144-3p调节的[具体基因名称]与GC的不良预后和巨噬细胞浸润相关。这可能是GC中的一种新生物标志物和治疗靶点。
