Zunyi Medical University, Department of Genetics, Guizhou, China.
Special Key Laboratory of Oral Disease Research and High Education Institute in Guizhou Province, Guizhou, China.
PeerJ. 2022 May 17;10:e13369. doi: 10.7717/peerj.13369. eCollection 2022.
The expression of ERGIC3 is increased in a variety of tumors and promotes the growth and metastasis of liver cancer, but the molecular mechanism needs to be further studied.In this study, we aimed to analyze the molecular mechanism of ERGIC3 regulating the proliferation of human hepatocellular carcinoma (HCC) SMMC-7721 cells using transcriptomics.
ERGIC3 was knocked down in SMMC-7721 cells by RNAi technique, and the expression of ERGIC3 was detected by Q-RT-PCR and Western Blot. RNA sequencing was performed in the Illumina HiSeq platform in the control group and the ERGIC3i group and bioinformatics methods were selected to analyze the data.
The expression of ERGIC3 was reduced to 10% in SMMC-7721 cells by RNAi technique, and 176 genes were up-regulated and 34 genes were down-regulated in ERGIC3i group compared with the control group. Analysis of the pathways and biological processes that enrich the function of differentially expressed genes showed thatthese differentially expressed genes were mainly involved in vesicular transport, growth factors, PI3K-Akt, NOD-like, Jak-STAT, NF-kappa B and other protein kinase-coupled receptors mediated signal transduction pathways, tumor immune response, collagen-integrin receptor-actin axis, and miRNA pathways. More importantly, most of the significantly altered pathways were related to immunity. ERGIC3 may be a key immune-related gene.
Based on the transcriptomic analysis, the mechanism of ERGIC3 promoting the growth of HCC is link with the transport of growth factor receptor, cytokine receptor and collagen. Then it is involved in signal transduction pathways mediated by protein kinase-coupled receptors, PI3K-Akt, NOD-like, Jak-STAT and NF-kappa B. In particular, the mechanism is also involved in the ERGIC3-dependent immune pathways. ERGIC3 is a potential target for prevention and treatment of HCC.
ERGIC3 在多种肿瘤中表达增加，促进肝癌的生长和转移，但分子机制仍需进一步研究。本研究旨在通过转录组学分析 ERGIC3 调节人肝癌 SMMC-7721 细胞增殖的分子机制。
采用 RNAi 技术敲低 SMMC-7721 细胞中的 ERGIC3，通过 Q-RT-PCR 和 Western blot 检测 ERGIC3 的表达。在对照组和 ERGIC3i 组的 Illumina HiSeq 平台上进行 RNA 测序，并选择生物信息学方法分析数据。
RNAi 技术使 SMMC-7721 细胞中 ERGIC3 的表达降低至 10%，与对照组相比，ERGIC3i 组中有 176 个基因上调，34 个基因下调。对差异表达基因功能富集分析的通路和生物过程表明，这些差异表达基因主要涉及囊泡运输、生长因子、PI3K-Akt、NOD 样、Jak-STAT、NF-kappa B 和其他蛋白激酶偶联受体介导的信号转导通路、肿瘤免疫反应、胶原-整合素受体-肌动蛋白轴和 miRNA 通路。更重要的是，大多数显著改变的通路与免疫有关。ERGIC3 可能是一个关键的免疫相关基因。
基于转录组学分析，ERGIC3 促进 HCC 生长的机制与生长因子受体、细胞因子受体和胶原的运输有关。然后，它参与了由蛋白激酶偶联受体、PI3K-Akt、NOD 样、Jak-STAT 和 NF-kappa B 介导的信号转导通路。特别是，该机制还涉及 ERGIC3 依赖性免疫通路。ERGIC3 是预防和治疗 HCC 的潜在靶点。
