Purpose: 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.
Methods: IDNK  expression was suppressed using short hairpin (shRNA) in BEL-7404 and Huh-7 cells. The expression of IDNK  in HCC cells after IDNK  knockdown was evaluated by real-time quantitative RT-PCR analysis and Western blot. After IDNK  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 IDNK  were identified, followed by pathway analysis.
Results: The expression of IDNK  at the mRNA and protein levels was considerably reduced in shRNA IDNK transfected cells. Knockdown of IDNK  significantly inhibited HCC cell proliferation and increased cell apoptosis. A total of 1196 genes (585 upregulated and 611 downregulated) were differentially expressed in IDNK  knockdown BEL-7404 cells. The pathway of tRNA charging with Z-score = − 3 was significantly inhibited in BEL-7404 cells with IDNK  knockdown.
Conclusion: IDNK  plays a key role in the proliferation and apoptosis of HCC cells. IDNK  may be a candidate therapeutic target for HCC.
Keywords: hepatocellular carcinoma cells, shRNA IDNK, cell proliferation, cell apoptosis, microarray, differentially expressed gene