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Deprecated: Implicit conversion from float 298.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Oncotarget 2015 ; 6 (42): 44660-74 Nephropedia Template TP
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Mutant p53 induces EZH2 expression and promotes epithelial?mesenchymal transition by disrupting p68-Drosha complex assembly and attenuating miR-26a processing #MMPMID26587974
Jiang FZ; He YY; Wang HH; Zhang HL; Zhang J; Yan XF; Wang XJ; Che Q; Ke JQ; Chen Z; Tong H; Zhang YL; Wang FY; Li YR; Wan XP
Oncotarget 2015[Dec]; 6 (42): 44660-74 PMID26587974show ga
The tumor suppressor p53 and the transcriptional repressor Enhancer of Zeste Homolog 2 (EZH2) have both been implicated in the regulation of epithelial-mesenchymal transition (EMT) and tumor metastasis via their impacts on microRNA expression. Here, we report that mutant p53 (mutp53) promotes EMT in endometrial carcinoma (EC) by disrupting p68-Drosha complex assembly. Overexpression of mutp53 has the opposite effect of wild-type p53 (WTp53), repressing miR-26a expression by reducing pri-miR-26a-1 processing in p53-null EC cells. Re-expression of miR-26a in mutp53 EC cells decreases cell invasion and promotes mesenchymal-epithelial transition (MET). Rescuing miR-26a expression also inhibits EZH2, N-cadherin, Vimentin, and Snail expression and induces E-cadherin expression both in vitro and in vivo. Moreover, patients with higher serum miR-26a levels have a better survival rate. These results suggest that p53 gain-of-function mutations accelerate EC tumor progression and metastasis by interfering with Drosha and p68 binding and pri-miR-26a-1 processing, resulting in reduced miR-26a expression and EZH2 overexpression.