Published online Dec 7, 2016. doi: 10.3748/wjg.v22.i45.9933
Peer-review started: August 27, 2016
First decision: September 6, 2016
Revised: September 30, 2016
Accepted: November 12, 2016
Article in press: November 16, 2016
Published online: December 7, 2016
Processing time: 103 Days and 18.8 Hours
Hepatocellular carcinoma (HCC) is one of the most lethal cancers, and its rate of incidence is rising annually. Despite the progress in diagnosis and treatment, the overall prognoses of HCC patients remain dismal due to the difficulties in early diagnosis and the high level of tumor invasion, metastasis and recurrence. It is urgent to explore the underlying mechanism of HCC carcinogenesis and progression to find out the specific biomarkers for HCC early diagnosis and the promising target for HCC chemotherapy. Recently, the reprogramming of cancer metabolism has been identified as a hallmark of cancer. The shift from the oxidative phosphorylation metabolic pathway to the glycolysis pathway in HCC meets the demands of rapid cell proliferation and offers a favorable microenvironment for tumor progression. Such metabolic reprogramming could be considered as a critical link between the different HCC genotypes and phenotypes. The regulation of metabolic reprogramming in cancer is complex and may occur via genetic mutations and epigenetic modulations including oncogenes, tumor suppressor genes, signaling pathways, noncoding RNAs, and glycolytic enzymes etc. Understanding the regulatory mechanisms of glycolysis in HCC may enrich our knowledge of hepatocellular carcinogenesis and provide important foundations in the search for novel diagnostic biomarkers and promising therapeutic targets for HCC.
Core tip: The reprogramming of glucose metabolism is one of the peculiar characteristics of cancer cells. This paper addresses the regulatory mechanism of glucose metabolism in hepatocellular carcinoma (HCC) and prospects its future application for HCC treatment.