Wu Xiao-Min, Jin Cheng, Gu Yuan-Long, Chen Wu-Qiang, Zhu Mao-Qun, Zhang Shuo, Zhang Zhen
Department of Integrated Traditional Chinese and Western Medicine Oncology, Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu 214062, People's Republic of China.
Department of Hepatobiliary Surgery, Affiliated Hospital of Jiangnan University, Wuxi, Jiangsu 214041, People's Republic of China.
Onco Targets Ther. 2020 Feb 26;13:1767-1776. doi: 10.2147/OTT.S234055. eCollection 2020.
Hepatocellular carcinoma (HCC) is one of the deadliest cancers globally with a poor prognosis. Breakthroughs in the treatment of HCC are urgently needed. This study explored the role of IDNK in the development and progression of HCC.
expression was suppressed using short hairpin (shRNA) in BEL-7404 and Huh-7 cells. The expression of in HCC cells after knockdown was evaluated by real-time quantitative RT-PCR analysis and Western blot. After silencing, the proliferation and apoptosis of HCC cells were evaluated by Celigo cell counting, flow cytometry analysis, MTT assay, and caspase3/7 assay. Gene expressions in BEL-7404 cells transfected with IDNK shRNA lentivirus plasmid and blank control plasmid were evaluated by microarray analysis. The differentially expressed genes induced by deregulation of were identified, followed by pathway analysis.
The expression of at the mRNA and protein levels was considerably reduced in shRNA IDNK transfected cells. Knockdown of significantly inhibited HCC cell proliferation and increased cell apoptosis. A total of 1196 genes (585 upregulated and 611 downregulated) were differentially expressed in knockdown BEL-7404 cells. The pathway of tRNA charging with Z-score = -3 was significantly inhibited in BEL-7404 cells with knockdown.
plays a key role in the proliferation and apoptosis of HCC cells. may be a candidate therapeutic target for HCC.
肝细胞癌（HCC）是全球最致命的癌症之一，预后较差。迫切需要在HCC治疗方面取得突破。本研究探讨了IDNK在HCC发生发展中的作用。
在BEL-7404和Huh-7细胞中使用短发夹RNA（shRNA）抑制其表达。通过实时定量RT-PCR分析和蛋白质印迹法评估敲低后HCC细胞中IDNK的表达。沉默IDNK后，通过Celigo细胞计数、流式细胞术分析、MTT法和caspase3/7法评估HCC细胞的增殖和凋亡。通过微阵列分析评估用IDNK shRNA慢病毒质粒和空白对照质粒转染的BEL-7404细胞中的基因表达。鉴定由IDNK失调诱导的差异表达基因，随后进行通路分析。
在转染shRNA IDNK的细胞中，IDNK的mRNA和蛋白质水平表达显著降低。敲低IDNK显著抑制HCC细胞增殖并增加细胞凋亡。在敲低IDNK的BEL-7404细胞中共有1196个基因（585个上调和611个下调）差异表达。在敲低IDNK的BEL-7404细胞中Z分数=-3的tRNA充电通路被显著抑制。
IDNK在HCC细胞的增殖和凋亡中起关键作用。IDNK可能是HCC的一个候选治疗靶点。
