<p>Gluconokinase IDNK Promotes Cell Proliferation and Inhibits Apoptosis in Hepatocellular Carcinoma</p>

Abstract

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 IDNKwere 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.

A fingerprint of 2-[18F]FDG radiometabolites – How tissue-specific metabolism beyond 2-[18F]FDG-6-P could affect tracer accumulation

“…Another, less likely possibility is the existence of an unknown secondary pathway for 2-[ 18 F]FDG entry at this step, such as oxidation to form fluorinated gluconate, which could be phosphorylated to form 2-[ 18 F]FD-PG1 independently of G6PD/H6PD. 53 , 54 …”