Department Of Hepatobiliary And Pancreatic Surgery, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian, China.
Department of Hepatobiliary and Pancreatic Surgery, QuanZhou Women's and Children's Hospital, Quanzhou, Fujian, China.
Cell Cycle. 2021 Oct;20(20):2114-2124. doi: 10.1080/15384101.2021.1962632. Epub 2021 Oct 6.
Being one of the most prevalent malignancies, hepatocellular carcinoma (HCC) threatens the health of population all over the world. Numerous researches have confirmed that long noncoding RNAs (lncRNAs) play an important role in tumor progression. Nonetheless, the mechanisms of unc-5 netrin receptor B antisense RNA 1 (UNC5B-AS1) in HCC remain obscure. Thus, this study aims to investigate the regulatory role and mechanism of UNC5B-AS1 in HCC cells. In our research, UNC5B-AS1 was subjected to gene expression analysis by RT-qPCR. Biological functions of UNC5B-AS1 in HCC cells were measured by MTT, colony formation, EdU and transwell assays. The combination between UNC5B-AS1, lysine demethylase 2A (KDM2A) and miR-4306 was validated by mechanism assays. Result showed UNC5B-AS1 was upregulated in HCC tissues and cells, contributing to the development of cancer staging and survival rate of HCC patients. Moreover, UNC5B-AS1 deficiency inhibited the proliferation, migration and epithelial-mesenchymal transition (EMT) of HCC cells. Furthermore, UNC5B-AS1 could interact with miR-4306 in HCC cells. Similarly, KDM2A was proved as the target gene of miR-4306. Finally, miR-4306 downregulation or KDM2A overexpression reversed the prohibitive role of UNC5B-AS1 knockdown in HCC progression. In short, UNC5B-AS1 accelerates the proliferation, migration and EMT of HCC cells via the regulation of miR-4306/KDM2A axis.
作为最常见的恶性肿瘤之一，肝细胞癌（HCC）威胁着全球人口的健康。大量研究证实，长链非编码 RNA（lncRNA）在肿瘤进展中发挥重要作用。然而，UNC5B-AS1 在 HCC 中的作用机制尚不清楚。因此，本研究旨在探讨 UNC5B-AS1 在 HCC 细胞中的调控作用及其机制。在我们的研究中，通过 RT-qPCR 进行基因表达分析。通过 MTT、集落形成、EdU 和 Transwell 测定来测量 UNC5B-AS1 在 HCC 细胞中的生物学功能。通过机制测定验证 UNC5B-AS1、赖氨酸去甲基酶 2A（KDM2A）和 miR-4306 之间的结合。结果显示 UNC5B-AS1 在 HCC 组织和细胞中上调，促进癌症分期和 HCC 患者生存率的发展。此外，UNC5B-AS1 缺乏抑制 HCC 细胞的增殖、迁移和上皮-间充质转化（EMT）。此外，UNC5B-AS1 可以与 HCC 细胞中的 miR-4306 相互作用。同样，KDM2A 被证明是 miR-4306 的靶基因。最后，miR-4306 的下调或 KDM2A 的过表达逆转了 UNC5B-AS1 敲低对 HCC 进展的抑制作用。总之，UNC5B-AS1 通过调节 miR-4306/KDM2A 轴加速 HCC 细胞的增殖、迁移和 EMT。
