Abstract：
:Gluconeogenesis is a fundamental feature of hepatocytes. Whether this gluconeogenic activity is also present in malignant hepatocytes remains unexplored. A better understanding of this biological process may lead to novel therapeutic strategies. Here we show that gluconeogenesis is not present in mouse or human malignant hepatocytes. We find that two critical enzymes 11β-HSD1 and 11β-HSD2 that regulate glucocorticoid activities are expressed inversely in malignant hepatocytes, resulting in the inactivation of endogenous glucocorticoids and the loss of gluconeogenesis. In patients' hepatocarcinoma, the expression of 11β-HSD1 and 11β-HSD2 is closely linked to prognosis and survival. Dexamethasone, an active form of synthesized glucocorticoids, is capable of restoring gluconeogenesis in malignant cells by bypassing the abnormal regulation of 11β-HSD enzymes, leading to therapeutic efficacy against hepatocarcinoma. These findings clarify the molecular basis of malignant hepatocyte loss of gluconeogenesis and suggest new therapeutic strategies.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Ma R,Zhang W,Tang K,Zhang H,Zhang Y,Li D,Li Y,Xu P,Luo S,Cai W,Ji T,Katirai F,Ye D,Huang Bdoi
10.1038/ncomms3508subject
Has Abstractpub_date
2013-01-01 00:00:00pages
2508issn
2041-1723pii
ncomms3508journal_volume
4pub_type
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