Abstract：
:The Warburg effect is a prominent metabolic feature associated with neoplastic diseases; however, the underlying mechanism remains incompletely understood. TAp73, a structural homolog of the tumor suppressor p53, is frequently overexpressed in human tumors, indicating a proliferative advantage that it can confer to tumor cells. Here we show that TAp73 stimulates the expression of phosphofructokinase-1, liver type (PFKL), which catalyzes the committed step in glycolysis. Through this regulation, TAp73 enhances glucose consumption and lactate excretion, promoting the Warburg effect. By activating PFKL, TAp73 also increases ATP production and bolsters anti-oxidant defense. TAp73 deficiency results in a pronounced reduction in tumorigenic potential, which can be rescued by forced PFKL expression. These findings establish TAp73 as a critical regulator of glycolysis and reveal a mechanism by which tumor cells achieve the Warburg effect to enable oncogenic growth.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Li L,Li L,Li W,Chen T,Bin Zou,Zhao L,Wang H,Wang X,Xu L,Liu X,Wang D,Li B,Mak TW,Du W,Yang X,Jiang Pdoi
10.1038/s41467-018-07127-8subject
Has Abstractpub_date
2018-11-08 00:00:00pages
4683issue
1issn
2041-1723pii
10.1038/s41467-018-07127-8journal_volume
9pub_type
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