ArticleCell death & disease2021
CSN6 promotes melanoma proliferation and metastasis by controlling the UBR5-mediated ubiquitination and degradation of CDK9.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Dendrimer-Derived Mimics of Host Defense Peptides Selectively Disrupt Cancer Cell Membranes for Melanoma Therapy.Pharmaceutics · 2025Article
- Tetrandrine targeting SIRT5 exerts anti-melanoma properties via inducing ROS, ER stress, and blocked autophagy.Journal of pharmaceutical analysis · 2024Article
- E3 ubiquitin ligase UBR5 modulates circadian rhythm by facilitating the ubiquitination and degradation of the key clock transcription factor BMAL1.Acta pharmacologica Sinica · 2024Article
- Mechanisms and potential applications of COPS6 in pan-cancer therapy.World journal of clinical oncology · 2024Article
- Comprehensive pan-cancer analysis reveals SIRT5 is a predictive biomarker for prognosis and immunotherapy response.Functional & integrative genomics · 2024Article
- Article
- Friend or foe? Reciprocal regulation between E3 ubiquitin ligases and deubiquitinases.Biochemical Society transactions · 2024Review
- Immune escape and metastasis mechanisms in melanoma: breaking down the dichotomy.Frontiers in immunology · 2024Review
- Computational exploration of the significance ofWorld journal of clinical oncology · 2023Article
- Evaluation of drug sensitivity, immunological characteristics, and prognosis in melanoma patients using an endoplasmic reticulum stress-associated signature based on bioinformatics and pan-cancer analysis.Journal of molecular medicine (Berlin, Germany) · 2023Article
- COPS6 promotes tumor progression and reduces CD8Acta pharmacologica Sinica · 2023Article
- UBE2S interacting with TRIM21 mediates the K11-linked ubiquitination of LPP to promote the lymphatic metastasis of bladder cancer.Cell death & disease · 2023Article
- CDK9 inhibitors downregulate DKK1 expression to suppress the metastatic potential of HCC cells.Genes & genomics · 2023Article
- SH3BP1 Regulates Melanoma Progression Through Race1/Wace2 Signaling Pathway.Clinical Medicine Insights. Oncology · 2023Article
- UBR5 targets tumor suppressor CDC73 proteolytically to promote aggressive breast cancer.Cell death & disease · 2022Article
- Targeting CDK9 for Anti-Cancer Therapeutics.Cancers · 2021Review
- Targeted Nanotherapeutics Using LACTB Gene Therapy Against Melanoma.International journal of nanomedicine · 2021Article
Corrections and comments
- Retraction · 2025-07-24Concerns/Issues about Data · Duplication of/in Image · Error in Image · Euphemisms for Duplication · Investigation by Journal/Publisher · Unreliable Data · · See also: https://pubpeer.com/publications/4F24B00948D70B709625A9430A30FC
- Retracted
Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.