To date, the anti-tumor mechanism of the deleted in liver cancer 2 (DLC2) in gliomas is still unclear. The study shows that TAp73α expression and TAp73α/TAp73β ratio are frequently high in gliomas and that TAp73α and TAp73β have opposite roles in regulating proliferation and apoptosis of glioma cells. Moreover, DLC2 is low-expressed in gliomas, which negatively correlates with TAp73α expression and TAp73α/TAp73β ratio. More importantly, DLC2 inhibits development of glioma by decreasing expression of TAp73α, which changes the expression ratio of TAp73α/TAp73β in glioma cells. Mechanically, DLC2 interacts directly with TAp73α and induces TAp73α ubiquitination and degradation, which is mediated through SAM domain of DLC2 and TAp73α. In detail, DLC2 with SAM domain deletion fails to interact with TAp73α and induce TAp73α ubiquitination and degradation, and SAM deletion decreased tumorigenesis-inhibition effect of DLC2. In conclusion, DLC2 inhibits glioma development by inducing TAp73α degradation and subsequent change of TAp73α/TAp73β expression ratio.
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