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Tat-Activating Regulatory DNA-Binding Protein Regulates Glycolysis in Hepatocellular Carcinoma by Regulating the Platelet Isoform of Phosphofructokinase Through MicroRNA 520

Authors
Park, Yun-YongKim, Sang-BaeHan, Hee DongSohn, Bo HwaKim, Ji HoonLiang, JiyongLu, YilingRodriguez-Aguayo, CristianLopez-Berestein, GabrielMills, Gordon B.Sood, Anil K.Lee, Ju-Seog
Issue Date
7월-2013
Publisher
WILEY
Citation
HEPATOLOGY, v.58, no.1, pp.182 - 191
Indexed
SCIE
SCOPUS
Journal Title
HEPATOLOGY
Volume
58
Number
1
Start Page
182
End Page
191
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/102814
DOI
10.1002/hep.26310
ISSN
0270-9139
Abstract
Metabolic changes are common features of many cancer cells and are frequently associated with the clinical outcome of patients with various cancers, including hepatocellular carcinoma (HCC). Thus, aberrant metabolic pathways in cancer cells are attractive targets for cancer therapy. However, our understanding of cancer-specific regulatory mechanisms of cell metabolism is still very limited. We found that Tat-activating regulatory DNA-binding protein (TARDBP) is a novel regulator of glycolysis in HCC cells. TARDBP regulates expression of the platelet isoform of phosphofructokinase (PFKP), the rate-limiting enzyme of glycolysis that catalyzes the irreversible conversion of fructose-6-phosphate to fructose-1,6-bisphosphate. Silencing of TARDBP expression in multiple HCC cell lines leads to impaired glucose metabolism and inhibition of in vitro and in vivo growth of HCC cells. Notably, the microRNA 520 (miR-520) family is an intermediate regulator of TARDBP-mediated regulation of glycolysis. Mechanistically, TARDBP suppressed expression of the miR-520 family, which, in turn, inhibited expression of PFKP. We further showed that expression of TARDBP is significantly associated with the overall survival of patients with HCC. Conclusion: Our study provides new mechanistic insights into the regulation of glycolysis in HCC cells and reveals TARDBP as a potential therapeutic target for HCC.
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