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csn, melanoma, cells, cdk, cell, expression, pubmed, article, ubr, csnknockdown, google, scholar, fig, cas, cancer, analysis, proliferation, ubiquitination, degradation, protein, invasion, central, performed, migration, assay, western, shcsn, found, control, china, nature, assays, liu, ligase, tumor, study, rescued, antibodies, metastasis, stability, data, cop, progression, cycle, samples, subunit, showed, results, blot, lysates,

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nature portfolio privacy policy medical research institute technology research centre nature advertising nl/cgi-bin/r2/main akt-csn6-myc signaling axis social media supplementary table 2 multi-tasking p-tefb complex reducing wnt/β-catenin signaling reprints csn6-ubr5-cdk9 axis promotes ubr5-knockdown csn6-knockdown group japan ubr5-knockdown csn6-knockdown a375 stably transfected csn6-knockdown csn6-rescued csn6-knockdown cells csn6-rescued csn6-knockdown a375 colorectal cancer development cullin-ring-ubiquitin ligases t-type cyclin/cdk9 complexes costimulatory molecule-related signature cdk9-mediated signaling pathways ice-cold pbs buffer 8-μm-pore transwell chambers state key laboratory csn6-knockdown cells counteracts mutant-type p53 protein csn6-silenced melanoma cells csn6-knockdown melanoma cells original author csn6/ubr5/cdk9 axis csn6-ubr5-cdk9 axis permissions potential csn6-interacting protein csn6-knockdown a375 cells patient data analysis quantitative real-time pcr e3 ubiquitin ligase cyclin-dependent kinase control reducing cop1 auto-ubiquitination pig1 cell line kaplan-meier survival analysis e-cadherin gene expression thyroid papillary cancer squamous cell cancers key transcriptional regulator colony formation ability

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         headline:CSN6 promotes melanoma proliferation and metastasis by controlling the UBR5-mediated ubiquitination and degradation of CDK9
         description:As a critical subunit of the constitutive photomorphogenesis 9 (COP9) signalosome (CSN), CSN6 is upregulated in some human cancers and plays critical roles in tumorigenesis and progression, but its biological functions and molecular mechanisms in melanoma remain unknown. Our study showed that CSN6 expression was upregulated in melanoma patients and cells, and correlated with poor survival in melanoma patients. In melanoma cells, CSN6 knockdown remarkably inhibited cell proliferation, tumorigenicity, migration, and invasion, whereas CSN6 recovery rescued the proliferative and metastatic abilities. Notably, we identified that CSN6 stabilized CDK9 expression by reducing CDK9 ubiquitination levels, thereby activating CDK9-mediated signaling pathways. In addition, our study described a novel CSN6-interacting E3 ligase UBR5, which was negatively regulated by CSN6 and could regulate the ubiquitination and degradation of CDK9 in melanoma cells. Furthermore, in CSN6-knockdown melanoma cells, UBR5 knockdown abrogated the effects caused by CSN6 silencing, suggesting that CSN6 activates the UBR5/CDK9 pathway to promote melanoma cell proliferation and metastasis. Thus, this study illustrates the mechanism by which the CSN6-UBR5-CDK9 axis promotes melanoma development, and demonstrate that CSN6 may be a potential biomarker and anticancer target in melanoma.
         datePublished:2021-01-22T00:00:00Z
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      headline:CSN6 promotes melanoma proliferation and metastasis by controlling the UBR5-mediated ubiquitination and degradation of CDK9
      description:As a critical subunit of the constitutive photomorphogenesis 9 (COP9) signalosome (CSN), CSN6 is upregulated in some human cancers and plays critical roles in tumorigenesis and progression, but its biological functions and molecular mechanisms in melanoma remain unknown. Our study showed that CSN6 expression was upregulated in melanoma patients and cells, and correlated with poor survival in melanoma patients. In melanoma cells, CSN6 knockdown remarkably inhibited cell proliferation, tumorigenicity, migration, and invasion, whereas CSN6 recovery rescued the proliferative and metastatic abilities. Notably, we identified that CSN6 stabilized CDK9 expression by reducing CDK9 ubiquitination levels, thereby activating CDK9-mediated signaling pathways. In addition, our study described a novel CSN6-interacting E3 ligase UBR5, which was negatively regulated by CSN6 and could regulate the ubiquitination and degradation of CDK9 in melanoma cells. Furthermore, in CSN6-knockdown melanoma cells, UBR5 knockdown abrogated the effects caused by CSN6 silencing, suggesting that CSN6 activates the UBR5/CDK9 pathway to promote melanoma cell proliferation and metastasis. Thus, this study illustrates the mechanism by which the CSN6-UBR5-CDK9 axis promotes melanoma development, and demonstrate that CSN6 may be a potential biomarker and anticancer target in melanoma.
      datePublished:2021-01-22T00:00:00Z
      dateModified:2021-01-22T00:00:00Z
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         Melanoma
         Oncogenes
         Skin stem cells
         Target identification
         Targeted therapies
         Life Sciences
         general
         Biochemistry
         Cell Biology
         Immunology
         Cell Culture
         Antibodies
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            address:
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               type:PostalAddress
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            address:
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      name:State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China
      name:Cancer center, Medical Research Institute, Southwest University, Chongqing, China
      name:Chongqing Engineering and Technology Research Centre for Silk Biomaterials and Regenerative Medicine, Chongqing, China
      name:Engineering Research Center for Cancer Biomedical and Translational Medicine, Southwest University, Chongqing, China
      name:Department of Dermatology, The Third Hospital of Hebei Medical University, Shijiazhuang, China
      name:State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China
      name:Department of Dermatology, The Third Hospital of Hebei Medical University, Shijiazhuang, China
      name:State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China
      name:State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China
      name:Cancer center, Medical Research Institute, Southwest University, Chongqing, China
      name:Chongqing Engineering and Technology Research Centre for Silk Biomaterials and Regenerative Medicine, Chongqing, China
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      name:Chongqing Engineering and Technology Research Centre for Silk Biomaterials and Regenerative Medicine, Chongqing, China
      name:Engineering Research Center for Cancer Biomedical and Translational Medicine, Southwest University, Chongqing, China
      name:Department of Dermatology, The Third Hospital of Hebei Medical University, Shijiazhuang, China
      name:State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China
      name:Department of Dermatology, The Third Hospital of Hebei Medical University, Shijiazhuang, China
      name:State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China
      name:Department of Dermatology, The Third Hospital of Hebei Medical University, Shijiazhuang, China
      name:State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, China
      name:Department of Dermatology, The Third Hospital of Hebei Medical University, Shijiazhuang, China
      name:Department of Dermatology, The Third Hospital of Hebei Medical University, Shijiazhuang, China
      name:Department of Dermatology, The Third Hospital of Hebei Medical University, Shijiazhuang, China
      name:Department of Dermatology, The Third Hospital of Hebei Medical University, Shijiazhuang, China
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