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- W2883676103 abstract "Inactivation of the von Hippel-Lindau (VHL) E3 ubiquitin ligase protein is a hallmark of clear cell renal cell carcinoma (ccRCC). Identifying how pathways affected by VHL loss contribute to ccRCC remains challenging. We used a genome-wide in vitro expression strategy to identify proteins that bind VHL when hydroxylated. Zinc fingers and homeoboxes 2 (ZHX2) was found as a VHL target, and its hydroxylation allowed VHL to regulate its protein stability. Tumor cells from ccRCC patients with VHL loss-of-function mutations usually had increased abundance and nuclear localization of ZHX2. Functionally, depletion of ZHX2 inhibited VHL-deficient ccRCC cell growth in vitro and in vivo. Mechanistically, integrated chromatin immunoprecipitation sequencing and microarray analysis showed that ZHX2 promoted nuclear factor κB activation. These studies reveal ZHX2 as a potential therapeutic target for ccRCC." @default.
- W2883676103 created "2018-08-03" @default.
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- W2883676103 date "2018-07-20" @default.
- W2883676103 modified "2023-10-09" @default.
- W2883676103 title "VHL substrate transcription factor ZHX2 as an oncogenic driver in clear cell renal cell carcinoma" @default.
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- W2883676103 doi "https://doi.org/10.1126/science.aap8411" @default.
- W2883676103 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6154478" @default.
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- W2883676103 hasPublicationYear "2018" @default.
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