| Literature DB >> 31043707 |
Dian Jiao1, Yi Huan2, Jia Zheng3, Ming Wei4, Guoxu Zheng5, Donghui Han6, Jieheng Wu7, Wenjin Xi7, Feilong Wei8, An-Gang Yang7, Weijun Qin9, He Wang10, Weihong Wen11.
Abstract
UHRF1 is an important epigenetic regulator that belongs to the UHRF family. Overexpression of UHRF1 has been found in many kinds of tumors and its overexpression is associated with poor prognosis and short survival in certain cancer types. However, its function in renal cell carcinoma (RCC) is not clear. Here we report that RCC tumor tissues had obviously higher UHRF1 expression than normal renal tissues. Downregulation of UHRF1 by siRNA or shRNA in RCC cell lines resulted in decreased cell viability, inhibited cell migration and invasion, and increased apoptosis. UHRF1 knockdown RCC xenografts also resulted in obviously inhibited tumor growth in vivo. After downregulation of UHRF1 in RCC cells, the expression of TXNIP was upregulated. In addition, after UHRF1 and TXNIP were simultaneously downregulated, cell viability and cell invasion increased, whereas cell apoptosis decreased compared with UHRF1 single downregulated cells. We also showed that UHRF1 could recruit HDAC1 to the TXNIP promoter and mediate the deacetylation of histone H3K9, resulting in the inhibition of TXNIP expression. Our results confirm that UHRF1 has oncogenic function in RCC and UHRF1 may promote tumor progression through epigenetic regulation of TXNIP. UHRF1 might be used as a therapeutic target for RCC treatment.Entities:
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Year: 2019 PMID： 31043707 DOI： 10.1038/s41388-019-0822-6
Source DB: PubMed Journal: Oncogene ISSN： 0950-9232 Impact factor: 9.867