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10.18632/oncotarget.4111 http://scihub22266oqcxt.onion/10.18632/oncotarget.4111 C4653025!4653025 !26244872     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26244872 &cmd=llinks): Failed to open stream: HTTP request failed! 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Jak3, STAT3, and STAT5 inhibit expression of miR-22, a novel tumor suppressor microRNA, in cutaneous T-Cell lymphoma |pdf=|usr=}}{{26244872 }} gab.com Text Jak3, STAT3, and STAT5 inhibit expression of miR-22, a novel tumor suppressor microRNA, in cutaneous T-Cell lymphoma JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26244872 #FOAvip Aberrant activation of Janus kinase-3 (Jak3) and its key down-stream effectors, Signal Transducer and Activator of Transcription-3 (STAT3) and STAT5, is a key feature of malignant transformation in cutaneous T-cell lymphoma (CTCL). However, it remains only partially understood how Jak3/STAT activation promotes lymphomagenesis. Recently, non-coding microRNAs (miRNAs) have been implicated in the pathogenesis of this malignancy. Here, we show that (i) malignant T cells display a decreased expression of a tumor suppressor miRNA, miR-22, when compared to non-malignant T cells, (ii) STAT5 binds the promoter of the miR-22 host gene, and (iii) inhibition of Jak3, STAT3, and STAT5 triggers increased expression of pri-miR-22 and miR-22. Curcumin, a nutrient with anti-Jak3 activity and histone deacetylase inhibitors (HDACi) also trigger increased expression of pri-miR-22 and miR-22. Transfection of malignant T cells with recombinant miR-22 inhibits the expression of validated miR-22 targets including NCoA1, a transcriptional co-activator in others cancers, as well as HDAC6, MAX, MYCBP, PTEN, and CDK2, which have all been implicated in CTCL pathogenesis. In conclusion, we provide the first evidence that de-regulated Jak3/STAT3/STAT5 signalling in CTCL cells represses the expression of the gene encoding miR-22, a novel tumor suppressor miRNA. Twit Text FOAVip Jak3, STAT3, and STAT5 inhibit expression of miR-22, a novel tumor suppressor microRNA, in cutaneous T-Cell lymphoma ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26244872 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26244872 #FOAvip English Wikipedia <ref>{{Cite pmid|26244872 }}</ref> Jak3, STAT3, and STAT5 inhibit expression of miR-22, a novel tumor suppressor microRNA, in cutaneous T-Cell lymphoma #MMPMID26244872 Sibbesen NA ; Kopp KL ; Litvinov IV ; Jønson L ; Willerslev-Olsen A ; Fredholm S ; Petersen DL ; Nastasi C ; Krejsgaard T ; Lindahl LM ; Gniadecki R ; Mongan NP ; Sasseville D ; Wasik MA ; Iversen L ; Bonefeld CM ; Geisler C ; Woetmann A ; Odum N Oncotarget 2015[Aug]; 6 (24 ): 20555-69 PMID26244872 show ga Aberrant activation of Janus kinase-3 (Jak3) and its key down-stream effectors, Signal Transducer and Activator of Transcription-3 (STAT3) and STAT5, is a key feature of malignant transformation in cutaneous T-cell lymphoma (CTCL). However, it remains only partially understood how Jak3/STAT activation promotes lymphomagenesis. Recently, non-coding microRNAs (miRNAs) have been implicated in the pathogenesis of this malignancy. Here, we show that (i) malignant T cells display a decreased expression of a tumor suppressor miRNA, miR-22, when compared to non-malignant T cells, (ii) STAT5 binds the promoter of the miR-22 host gene, and (iii) inhibition of Jak3, STAT3, and STAT5 triggers increased expression of pri-miR-22 and miR-22. Curcumin, a nutrient with anti-Jak3 activity and histone deacetylase inhibitors (HDACi) also trigger increased expression of pri-miR-22 and miR-22. Transfection of malignant T cells with recombinant miR-22 inhibits the expression of validated miR-22 targets including NCoA1, a transcriptional co-activator in others cancers, as well as HDAC6, MAX, MYCBP, PTEN, and CDK2, which have all been implicated in CTCL pathogenesis. In conclusion, we provide the first evidence that de-regulated Jak3/STAT3/STAT5 signalling in CTCL cells represses the expression of the gene encoding miR-22, a novel tumor suppressor miRNA. |Cell Line, Tumor [MESH] |Genes, Tumor Suppressor [MESH] |Humans [MESH] |Janus Kinase 3/antagonists & inhibitors/genetics/*metabolism [MESH] |Lymphoma, T-Cell, Cutaneous/*genetics/metabolism/pathology [MESH] |MicroRNAs/administration & dosage/*antagonists & inhibitors/biosynthesis/genetics [MESH] |Piperidines/pharmacology [MESH] |Protein Kinase Inhibitors/pharmacology [MESH] |Pyrimidines/pharmacology [MESH] |Pyrroles/pharmacology [MESH] |STAT3 Transcription Factor/genetics/*metabolism [MESH] |STAT5 Transcription Factor/genetics/*metabolism [MESH] |Signal Transduction [MESH] |Skin Neoplasms/*genetics/metabolism/pathology [MESH]Jak3, STAT3, and STAT5 inhibit expression of miR-22, a novel tumor sup(epmc).pdf DeepDyve Pubget Overpricing