Department of Oncology, The Second Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China.
Eur Rev Med Pharmacol Sci. 2020 Oct;24(20):10452-10461. doi: 10.26355/eurrev_202010_23397.
LINC00240, as a novel long non-coding RNAs (lncRNAs), has never been studied in hepatocellular carcinoma (HCC). This research reported the expression and function of LINC00240 in HCC.
LINC00240 expression in 180 HCC patients was downloaded from the Cancer Genome Atlas (TCGA) database. HCC patients' survival was analyzed via Kaplan‑Meier analysis. The expression of LINC00240, miR-4465 and HGF in Hep3B and Huh7 cells were regulated by transfection. Cell viability was determined by MTT assay. Transwell experiment was used for the detection of cells migration and invasion abilities. The interaction between LINC00240, miR-4465 and HGF was reflected by Luciferase reporter assay. LINC00240, miR-4465, HGF and p-c-MET expression in HCC cells were researched by real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot.
TCGA data showed that high LINC00240 expression was markedly associated with lower survival of HCC patients (p = 0.036). LINC00240 expression was aberrantly upregulated in HCC cells. Silencing of LINC00240 significantly reduced HCC cells viability, migration and invasion. miR-4465 was a target gene of LINC00240. Silencing of LINC00240 reduced HCC cells viability, migration and invasion via directly promoting miR-4465 expression. HGF was target gene of miR-4465. miR-4465 up-regulation obviously suppressed HGF and p-c-MET expression. According to rescue experiment, LINC00240 silencing inhibited HCC cells viability, migration and invasion by suppressing HGF/c-MET signaling pathway via targeting miR-4465.
LINC00240 sponges miR-4465 to promote HCC cells proliferation, migration and invasion via HGF/c-MET signaling pathway.
LINC00240 作为一种新型长链非编码 RNA（lncRNA），尚未在肝细胞癌（HCC）中进行研究。本研究报道了 LINC00240 在 HCC 中的表达和功能。
从癌症基因组图谱（TCGA）数据库中下载了 180 例 HCC 患者的 LINC00240 表达数据。通过 Kaplan-Meier 分析对 HCC 患者的生存情况进行分析。通过转染调节 Hep3B 和 Huh7 细胞中 LINC00240、miR-4465 和 HGF 的表达。通过 MTT 测定法测定细胞活力。通过 Transwell 实验检测细胞迁移和侵袭能力。通过荧光素酶报告实验反映 LINC00240、miR-4465 和 HGF 之间的相互作用。通过实时定量聚合酶链反应（RT-qPCR）和 Western blot 研究 HCC 细胞中的 LINC00240、miR-4465、HGF 和 p-c-MET 的表达。
TCGA 数据表明，高 LINC00240 表达与 HCC 患者生存率降低显著相关（p=0.036）。LINC00240 在 HCC 细胞中表达异常上调。沉默 LINC00240 可显著降低 HCC 细胞活力、迁移和侵袭。miR-4465 是 LINC00240 的靶基因。沉默 LINC00240 通过直接促进 miR-4465 表达来降低 HCC 细胞活力、迁移和侵袭。HGF 是 miR-4465 的靶基因。miR-4465 的上调明显抑制了 HGF 和 p-c-MET 的表达。根据挽救实验，沉默 LINC00240 通过靶向 miR-4465 抑制 HCC 细胞活力、迁移和侵袭，抑制 HGF/c-MET 信号通路。
LINC00240 通过海绵 miR-4465 促进 HCC 细胞增殖、迁移和侵袭，通过 HGF/c-MET 信号通路。
