科研之友
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摘要
To date, the anti-tumor mechanism of the deleted in liver cancer 2 (DLC2) in gliomas is still unclear. The study shows that TAp73 alpha expression and TAp73 alpha/TAp73 beta ratio are frequently high in gliomas and that TAp73 alpha and TAp73 beta have opposite roles in regulating proliferation and apoptosis of glioma cells. Moreover, DLC2 is low-expressed in gliomas, which negatively correlates with TAp73 alpha expression and TAp73 alpha/TAp73 beta ratio. More importantly, DLC2 inhibits development of glioma by decreasing expression of TAp73 alpha, which changes the expression ratio of TAp73 alpha/TAp73 beta in glioma cells. Mechanically, DLC2 interacts directly with TAp73 alpha and induces TAp73 alpha ubiquitination and degradation, which is mediated through SAM domain of DLC2 and TAp73 alpha. In detail, DLC2 with SAM domain deletion fails to interact with TAp73 alpha and induce TAp73 alpha ubiquitination and degradation, and SAM deletion decreased tumorigenesis-inhibition effect of DLC2. In conclusion, DLC2 inhibits glioma development by inducing TAp73 alpha degradation and subsequent change of TAp73 alpha/TAp73 beta expression ratio.
