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miR-301b plays an oncogenic role in triple negative breast cancer (TNBC) possibly by downregulating CYLD and subsequently activating NF-kappaB p65, and this may provide a novel therapeutic approach for TNBC.
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Study revealed that miR-182 expression was significantly upregulated in human gastrointestinal stromal tumors (GISTs) compared with adjacent normal tissues. Overexpression of miR-182 enhanced GIST-T1 cell growth, with increased proliferation and decreased apoptosis. In addition, cylindromatosis (CYLD) was identified as a direct target of miR-182.
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A substantial number of CLL patient samples express sCYLD.
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No genotype-phenotype correlation was found in tumor disorders of the skin appendages associated with mutations in the CYLD gene.
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Catalytic domain mutation in CYLD gene is associated with osteosarcoma.
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Studied the role of maternally expressed 3 (lncRNA-MEG3) as an antitumor lncRNA for malignant melanoma by regulating miR-499-5p/CYLD axis.
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CYLD inhibits post-transcriptional regulation of RIG-I and MDA5 expression following TLR3 activation in MCs. CYLD may be involved in the pathogenesis of CKD
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miR-197-3p-induced downregulation of CYLD promotes cell proliferation and inhibits cell apoptosis in lung adenocarcinoma cell lines.
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Knockdown of CYLD expression reversed the cell proliferation promotion by miR1288in in glioblastoma.
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TNF phase III signalling displays ongoing TNFR1/NF-kappa B activation in monocytic cells. High- and low-sensitive genes are induced including differentially regulated A20. A20 strictly controls this signalling in an IKK- and partially RIP-dependent manner. The A20-mediated control mechanisms are supported by ABIN1 and CYLD.
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Low expression of CYLD is associated with glioma.
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theses data show that CYLD regulates the magnitude of ubiquitination of several major effectors of the EGFR pathway by assisting the recruitment of the ubiquitin ligase Cbl-b to the activated EGFR complex.
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Through deceasing the expression of Cylindromatosis (CYLD), a K63-specific DUB and endogenous blocker of NF-kappaB signaling, miR-130b can in return sustain the persistent activation of NF-kappaB, which may promote the malignant progression of transitional cell carcinoma of bladder.
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While previous reports have described CYLD as a regulator of DVL proteins; this data suggests the presence of a more complicated reciprocal regulatory mechanism in CML cell lines.
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Thrombin-mediated MALT1 protease activation triggers acute disruption of endothelial barrier integrity via CYLD cleavage.
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MiR-767 acted as a role of tumor promoter by targeting CYLD in human melanoma.
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SPATA2 has been described as a previously unrecognized factor in the linear ubiquitin chain assembly complex-dependent signaling pathways that serves as an adaptor between HOIP and CYLD, thereby enabling recruitment of CYLD to signaling complexes.
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The data reveal SPATA2 as a high-affinity binding partner of CYLD and HOIP, and a regulatory component of linear ubiquitin chain assembly complex-mediated NF-kappaB signaling.
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The current investigations identified a subset of HPV-positive HNSCCs with mutations in the genes TRAF3 (tumor necrosis factor receptor-associated factor 3) and CYLD (cylindromatosis lysine 63 deubiquitinase). Defects in TRAF3 and CYLD correlated with the activation of transcriptional factor nuclear factor kappaB, episomal HPV status of tumors, and improved patient survival.
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The predicted PUB domain in the N-terminus of SPATA2 interacts with the USP domain of CYLD and SPATA2 is required for recruitment of CYLD to the TNF-alpha receptor-associated signaling complexes.
