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10.1016/j.canlet.2015.03.037 http://scihub22266oqcxt.onion/10.1016/j.canlet.2015.03.037 C4406488!4406488 !25827072     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25827072 &cmd=llinks): Failed to open stream: HTTP request failed! 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FBXO11 promotes ubiquitination of the Snail family of transcription factors in cancer progression and epidermal development |pdf=|usr=}}{{25827072 }} gab.com Text FBXO11 promotes ubiquitination of the Snail family of transcription factors in cancer progression and epidermal development JO: Cancer Lett http://www.kidney.de/pget.php?&tw=1&pmid=25827072 #FOAvip The Snail family of transcription factors are core inducers of epithelial-to-mesenchymal transition (EMT). Here we show that the F-box protein FBXO11 recognizes and promotes ubiquitin-mediated degradation of multiple Snail family members including Scratch. The association between FBXO11 and Snai1 in vitro is independent of Snai1 phosphorylation. Overexpression of FBXO11 in mesenchymal cells reduces Snail protein abundance and cellular invasiveness. Conversely, depletion of endogenous FBXO11 in epithelial cancer cells causes Snail protein accumulation, EMT, and tumor invasion, as well as loss of estrogen receptor expression in breast cancer cells. Expression of FBXO11 is downregulated by EMT-inducing signals TGF? and nickel. In human cancer, high FBXO11 levels correlate with expression of epithelial markers and favorable prognosis. The results suggest that FBXO11 sustains the epithelial state and inhibits cancer progression. Inactivation of FBXO11 in mice leads to neonatal lethality, epidermal thickening, and increased Snail protein levels in epidermis, validating that FBXO11 is a physiological ubiquitin ligase of Snail. Moreover, in C. elegans, the FBXO11 mutant phenotype is attributed to the Snail factors as it is suppressed by inactivation/depletion of Snail homologs. Collectively, these findings suggest that the FBXO11-Snail regulatory axis is evolutionarily conserved and critically governs carcinoma progression and mammalian epidermal development. Twit Text FOAVip FBXO11 promotes ubiquitination of the Snail family of transcription factors in cancer progression and epidermal development ????Cancer Lett http://www.kidney.de/pget.php?&tw=1&pmid=25827072 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25827072 #FOAvip English Wikipedia <ref>{{Cite pmid|25827072 }}</ref> FBXO11 promotes ubiquitination of the Snail family of transcription factors in cancer progression and epidermal development #MMPMID25827072 Jin Y ; Shenoy AK ; Doernberg S ; Chen H ; Luo H ; Shen H ; Lin T ; Tarrash M ; Cai Q ; Hu X ; Fiske R ; Chen T ; Wu L ; Mohammed KA ; Rottiers V ; Lee SS ; Lu J Cancer Lett 2015[Jun]; 362 (1 ): 70-82 PMID25827072 show ga The Snail family of transcription factors are core inducers of epithelial-to-mesenchymal transition (EMT). Here we show that the F-box protein FBXO11 recognizes and promotes ubiquitin-mediated degradation of multiple Snail family members including Scratch. The association between FBXO11 and Snai1 in vitro is independent of Snai1 phosphorylation. Overexpression of FBXO11 in mesenchymal cells reduces Snail protein abundance and cellular invasiveness. Conversely, depletion of endogenous FBXO11 in epithelial cancer cells causes Snail protein accumulation, EMT, and tumor invasion, as well as loss of estrogen receptor expression in breast cancer cells. Expression of FBXO11 is downregulated by EMT-inducing signals TGF? and nickel. In human cancer, high FBXO11 levels correlate with expression of epithelial markers and favorable prognosis. The results suggest that FBXO11 sustains the epithelial state and inhibits cancer progression. Inactivation of FBXO11 in mice leads to neonatal lethality, epidermal thickening, and increased Snail protein levels in epidermis, validating that FBXO11 is a physiological ubiquitin ligase of Snail. Moreover, in C. elegans, the FBXO11 mutant phenotype is attributed to the Snail factors as it is suppressed by inactivation/depletion of Snail homologs. Collectively, these findings suggest that the FBXO11-Snail regulatory axis is evolutionarily conserved and critically governs carcinoma progression and mammalian epidermal development. |Animals [MESH] |Breast Neoplasms/*metabolism/pathology [MESH] |Caenorhabditis elegans [MESH] |Disease Progression [MESH] |Epidermis/growth & development/*metabolism [MESH] |Epithelial-Mesenchymal Transition [MESH] |F-Box Proteins/genetics/*metabolism [MESH] |Female [MESH] |Humans [MESH] |MCF-7 Cells [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Protein-Arginine N-Methyltransferases/genetics/*metabolism [MESH] |Snail Family Transcription Factors [MESH] |Transcription Factors/*metabolism [MESH]FBXO11 promotes ubiquitination of the Snail family of transcription fa(epmc).pdf DeepDyve Pubget Overpricing