Youjiang Medical University for Nationalities School of Laboratory Medicine, Baise, Guangxi, China.
Youjiang Medical University for Nationalities Graduate School, Baise, Guangxi, China.
Turk J Gastroenterol. 2024 Apr;35(4):307-315. doi: 10.5152/tjg.2024.23454.
BACKGROUND/AIMS: A large number of differentially expressed molecules exist in hepatocellular carcinoma (HCC), and the mechanism by which they upregulate or downregulate expression is still unclear. The purpose of this study is to explore the possible mechanism of differential expression of apoptotic chromatin condensation inducer 1 (Acin1) in HCC.
A mouse HCC model was constructed, and the expression of Acin1 in HCC was analyzed by whole transcriptome sequencing, bioinformatics analysis, and reverse transcription-quantitative polymerase chain reaction, and differentially expressed Acin1-related genes were screened to construct a protein-protein interaction and competing endogenous RNA (ceRNA) network. The microRNA (miRNAs) targeting Acin1 were further predicted using online databases and finally compared with sequencing data.
The expression of Acin1 was significantly up-regulated in HCC compared to the paracancerous and healthy control groups (P<.001). The top 10 upregulated genes closely related to Acin1 (Slc3a2, Wiz, Srrm2, Akt1, Hnrnpu, Sap18b, Pabpn1, Ddx39b, Eif4a3, and Rnps1) were mainly involved in pathways such as messenger RNA (mRNA) surveillance, RNA transport, spliceosome, Janus kinase/ signal transducers and activators of transcription signaling, apoptosis, and ubiquitin-mediated proteolysis. The ceRNA network identified several molecules (2 long noncoding RNAs, 50 miRNAs, and 49 mRNAs) interacting with Acin1, among which miR-674-5p was highly expressed in all sample tissues, and higher than that of other differentially expressed miRNAs, and significantly downregulated in HCC. Multiple online databases such as miRWalk also predicted that miR-674-5p targets Acin1. This shows that miR-674-5p may be an important molecule for targeting Acin1.
Acin1 is overexpressed in HCC, and the overexpressed Acin1 is most likely regulated by miR-674-5p and other ceRNA molecules.
背景/目的：肝细胞癌（HCC）中存在大量差异表达的分子，但其上调或下调表达的机制尚不清楚。本研究旨在探讨凋亡染色质凝聚诱导因子 1（Acin1）在 HCC 中差异表达的可能机制。
构建小鼠 HCC 模型，通过全转录组测序、生物信息学分析和逆转录定量聚合酶链反应分析 HCC 中 Acin1 的表达，并筛选差异表达的 Acin1 相关基因构建蛋白质-蛋白质相互作用和竞争内源性 RNA（ceRNA）网络。使用在线数据库进一步预测靶向 Acin1 的 microRNA（miRNA），最后与测序数据进行比较。
与癌旁和健康对照组相比，Acin1 在 HCC 中的表达明显上调（P<.001）。与 Acin1 密切相关的前 10 个上调基因（Slc3a2、Wiz、Srrm2、Akt1、Hnrnpu、Sap18b、Pabpn1、Ddx39b、Eif4a3 和 Rnps1）主要参与信使 RNA（mRNA）监测、RNA 转运、剪接体、Janus 激酶/信号转导和转录激活因子信号、凋亡和泛素介导的蛋白水解等途径。ceRNA 网络鉴定出与 Acin1 相互作用的几种分子（2 个长非编码 RNA、50 个 miRNA 和 49 个 mRNA），其中 miR-674-5p 在所有样本组织中均高度表达，且高于其他差异表达的 miRNA，在 HCC 中显著下调。miRWalk 等多个在线数据库预测 miR-674-5p 靶向 Acin1。这表明 miR-674-5p 可能是靶向 Acin1 的重要分子。
Acin1 在 HCC 中过度表达，过表达的 Acin1 很可能受 miR-674-5p 和其他 ceRNA 分子的调控。
