---
title: "CSN1 and the COP9 signalosome regulate glioblastoma stem cell growth and tumorigenesis"
id: "plos-one-4-the-cop9-signalosome-subunit-csn1-regulates-glioblastoma-stem-cell-growth"
canonical_url: "https://medichelpline.com/clinical-feed/plos-one-4-the-cop9-signalosome-subunit-csn1-regulates-glioblastoma-stem-cell-growth"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "PLOS ONE (Medicine)"
source_url: "https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568"
published_at: "2026-09-17T14:00:00.000Z"
evidence_level: "Journal Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# CSN1 and the COP9 signalosome regulate glioblastoma stem cell growth and tumorigenesis
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/plos-one-4-the-cop9-signalosome-subunit-csn1-regulates-glioblastoma-stem-cell-growth
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** PLOS ONE (Medicine)
- **Source URL:** [Original Journal Publication](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568)
- **Published At:** 2026-09-17T14:00:00.000Z
- **Evidence Rating:** Journal Feed
## Executive GIST (TL;DR)
- The COP9 signalosome is an eight-subunit complex that modulates the ubiquitin-proteasome system by de-neddylating Cullin-RING ubiquitin ligases; its role in glioblastoma was previously underexplored. - A genome-wide essentiality screen of 11 patient-derived glioblastoma stem cell (GSC) cultures identified GPS1 (CSN1) and COPS6 (CSN6) as the only COP9 subunit genes whose knockout reduced fitness across all lines. - CSN1 protein is broadly expressed across a panel of patient-derived GSC cultures. - CRISPR-Cas9 knockout of GPS1 (CSN1-KO) in two independent patient-derived GSC lines produced reduced or near-complete loss of CSN1 protein and markedly inhibited in vitro GSC growth over a 14-day period. - CSN1-KO caused cell cycle disruption with fewer cells in S and G2+M phases and accumulation in G0/G1, reduced EdU incorporation, decreased sphere-initiating frequency, and lower SOX2 expression, indicating impaired stemness. - Orthotopic xenografts of CSN1-KO GSCs in SCID mice produced a significant survival advantage compared with controls (log-rank p < 0.0001 in two independent GSC models). - RNA-sequencing and GSEA showed negative enrichment of cell cycle programs and positive enrichment of apoptosis-related genes in CSN1-KO GSCs versus controls. - CSN1 loss destabilized most COP9 subunits at the protein level (loss of CSN3, CSN5, CSN6, CSN7A/B, CSN8) while CSN2 and CSN4 were maintained or upregulated; transcriptional changes did not explain the protein loss, implicating post-translational destabilization. - Phospho-kinase array and validation blots revealed increased phosphorylation of STAT3 (Y705, S727), JNK1/2/3 (T183/Y185, T221/Y223), and c-Jun (S63) in CSN1-KO GSCs without corresponding increases in total protein levels. - Transcription factor target enrichment implicated **AP-1** target activation in CSN1-KO GSCs, consistent with increased JNK/c-Jun phosphorylation; AP-1 activation may contribute to observed transcriptional changes. - CSN1-KO cells did not show increased sensitivity to the JAK2/STAT3 inhibitor pacritinib at tested concentrations, suggesting STAT3 phosphorylation is not a dominant compensatory survival mechanism under those conditions. - Overall, CSN1 is essential for COP9 assembly, maintenance of the phospho-proteome, regulation of **AP-1** activity, and GSC proliferation and tumorigenesis. Data and original blots and RNA-seq deposits are listed in public repositories as reported.
## Clinical Analysis & Structured Key Points
[ Skip to main content ](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#main-content) Advertisement * [plos.org](https://plos.org/) * [Create account](https://community.plos.org/registration/new) * [Sign in](https://journals.plos.org/user/secure/login?page=%2Fplosone%2Farticle%3Fid%3D10.1371%2Fjournal.pone.0358568) * * About * Browse * Publish * [](https://journals.plos.org/plosone/ "PLOS One") * Search [advanced search](https://journals.plos.org/plosone/search) * [Browse Topics](https://journals.plos.org/plosone/subjectAreaBrowse) Browse Subject Areas ? Click through the PLOS taxonomy to find articles in your field. For more information about PLOS Subject Areas, click [here](https://github.com/PLOS/plos-thesaurus/blob/master/README.md "Link opens in new window"). [](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568) [](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568) * 0 [Save](https://journals.plos.org/plosone/article/metrics?id=10.1371/journal.pone.0358568#savedHeader) [Total Mendeley and Citeulike bookmarks.](https://journals.plos.org/plosone/article/metrics?id=10.1371/journal.pone.0358568#savedHeader) * 0 [Citation](https://journals.plos.org/plosone/article/metrics?id=10.1371/journal.pone.0358568#citedHeader) [Paper's citation count computed by Dimensions.](https://journals.plos.org/plosone/article/metrics?id=10.1371/journal.pone.0358568#citedHeader) * 0 [View](https://journals.plos.org/plosone/article/metrics?id=10.1371/journal.pone.0358568#viewedHeader) [PLOS views and downloads.](https://journals.plos.org/plosone/article/metrics?id=10.1371/journal.pone.0358568#viewedHeader) * 0 [Share](https://journals.plos.org/plosone/article/metrics?id=10.1371/journal.pone.0358568#discussedHeader) [Sum of Facebook, Twitter, Reddit and Wikipedia activity.](https://journals.plos.org/plosone/article/metrics?id=10.1371/journal.pone.0358568#discussedHeader) Open Access Peer-reviewed Research Article # The COP9 signalosome subunit CSN1 regulates glioblastoma stem cell growth * Samir Assaf, Roles Conceptualization, Data curation, Formal analysis, Investigation, Visualization, Writing – original draft Affiliations Arnie Charbonneau Cancer Institute, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada, Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada, Department of Cell Biology and Anatomy, University of Calgary, Calgary, Alberta, Canada ⨯ * Kyle Heemskerk, Roles Data curation, Formal analysis, Visualization Affiliations Arnie Charbonneau Cancer Institute, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada, Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada, Department of Cell Biology and Anatomy, University of Calgary, Calgary, Alberta, Canada ⨯ * Xiaoguang Hao, Roles Data curation, Formal analysis, Investigation, Visualization Affiliations Arnie Charbonneau Cancer Institute, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada, Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada, Department of Cell Biology and Anatomy, University of Calgary, Calgary, Alberta, Canada ⨯ * H. Artee Luchman, Roles Funding acquisition, Supervision, Writing – review & editing Affiliations Arnie Charbonneau Cancer Institute, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada, Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada, Department of Cell Biology and Anatomy, University of Calgary, Calgary, Alberta, Canada ⨯ * Samuel Weiss Roles Funding acquisition, Supervision, Writing – review & editing * E-mail: weiss@ucalgary.ca Affiliations Arnie Charbonneau Cancer Institute, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada, Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada, Department of Cell Biology and Anatomy, University of Calgary, Calgary, Alberta, Canada [ ![ORCID logo](https://journals.plos.org/resource/img/orcid_16x16.png) https://orcid.org/0009-0003-9190-563X ](https://orcid.org/0009-0003-9190-563X "ORCID Registry") ⨯ # The COP9 signalosome subunit CSN1 regulates glioblastoma stem cell growth * Samir Assaf, * Kyle Heemskerk, * Xiaoguang Hao, * H. Artee Luchman, * Samuel Weiss ![PLOS](https://journals.plos.org/resource/img/logo-plos-full-color.svg) x * Published: September 17, 2026 * * [Article](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568) * [Authors](https://journals.plos.org/plosone/article/authors?id=10.1371/journal.pone.0358568) * [Metrics](https://journals.plos.org/plosone/article/metrics?id=10.1371/journal.pone.0358568) * [Comments](https://journals.plos.org/plosone/article/comments?id=10.1371/journal.pone.0358568) * [Media Coverage](http://plos.altmetric.com/details/doi/10.1371/journal.pone.0358568) * [Abstract](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#abstract0) * [Introduction](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#sec001) * [Results](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#sec002) * [Discussion](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#sec007) * [Methods](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#sec008) * [Acknowledgments](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#ack) * [References](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#references) * [Reader Comments](https://journals.plos.org/plosone/article/comments?id=10.1371/journal.pone.0358568) * [Figures](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568) ## Abstract The COP9 signalosome is composed of 8 subunits (CSN1-CSN8) and plays a key role in regulating the activity of the ubiquitin-proteasome system by modulating Cullin-RING ubiquitin ligases. While the function of the COP9 signalosome in regulating protein homeostasis is well established, little is known about its role in glioblastoma. Here, using patient-derived glioblastoma stem cell lines, we identified CSN1 as a crucial COP9 signalosome subunit for _in vitro_ growth. CSN1 knockout was further found to significantly extend survival in orthotopic glioblastoma xenograft models. Transcriptomic analysis revealed that CSN1 knockout disrupted transcriptional programs involved in cell cycle progression and activated apoptotic pathways. Molecular analysis further determined that CSN1 is required for COP9 signalosome complex assembly and regulates AP-1 activation via JNK1/2/3 and c-Jun phosphorylation. These results highlight the essentiality of CSN1 for glioblastoma stem cell growth and provide insights into the cellular mechanisms controlled by CSN1 and the COP9 signalosome. ## Figures ![Fig 4](https://journals.plos.org/plosone/article/figure/image?size=inline&id=10.1371/journal.pone.0358568.g004) ![Fig 5](https://journals.plos.org/plosone/article/figure/image?size=inline&id=10.1371/journal.pone.0358568.g005) ![](https://journals.plos.org/plosone/article/figure/image?size=inline&id=10.1371/journal.pone.0358568.t001) ![Fig 1](https://journals.plos.org/plosone/article/figure/image?size=inline&id=10.1371/journal.pone.0358568.g001) ![Fig 2](https://journals.plos.org/plosone/article/figure/image?size=inline&id=10.1371/journal.pone.0358568.g002) ![Fig 3](https://journals.plos.org/plosone/article/figure/image?size=inline&id=10.1371/journal.pone.0358568.g003) ![Fig 4](https://journals.plos.org/plosone/article/figure/image?size=inline&id=10.1371/journal.pone.0358568.g004) ![Fig 5](https://journals.plos.org/plosone/article/figure/image?size=inline&id=10.1371/journal.pone.0358568.g005) ![](https://journals.plos.org/plosone/article/figure/image?size=inline&id=10.1371/journal.pone.0358568.t001) ![Fig 1](https://journals.plos.org/plosone/article/figure/image?size=inline&id=10.1371/journal.pone.0358568.g001) ![Fig 2](https://journals.plos.org/plosone/article/figure/image?size=inline&id=10.1371/journal.pone.0358568.g002) ![Fig 3](https://journals.plos.org/plosone/article/figure/image?size=inline&id=10.1371/journal.pone.0358568.g003) **Citation:** Assaf S, Heemskerk K, Hao X, Luchman HA, Weiss S (2026) The COP9 signalosome subunit CSN1 regulates glioblastoma stem cell growth. PLoS One 21(9): e0358568. https://doi.org/10.1371/journal.pone.0358568 **Editor:** Ryota Tamura, Keio University School of Medicine Graduate School of Medicine: Keio Gijuku Daigaku Igakubu Daigakuin Igaku Kenkyuka, JAPAN **Received:** March 16, 2026; **Accepted:** August 24, 2026; **Published:** September 17, 2026 **Copyright:** © 2026 Assaf et al. This is an open access article distributed under the terms of the [Creative Commons Attribution License](http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. **Data Availability:** RNA-sequencing data has been deposited in the NCBI Sequence Read Archive (SRA) database: PRJNA1497041 ([https://www.ncbi.nlm.nih.gov/bioproject/PRJNA1497041)](https://www.ncbi.nlm.nih.gov/bioproject/PRJNA1497041). The original representative Western blots have been deposited at Mendeley Data doi:10.17632/jyc4j3vkfk.1 ([https://data.mendeley.com/datasets/jyc4j3vkfk/1)](https://data.mendeley.com/datasets/jyc4j3vkfk/1). **Funding:** This study was supported by a grant from the Canadian Institutes for Health Research (153246 to H.A. Luchman, S. Weiss). The funders had no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. **Competing interests:** The authors have declared that no competing interests exist. ## Introduction Proteostasis is a vital system that ensures the balance of regulatory proteins in the cell is maintained, ultimately controlling critical functions and responses to external stimuli [[1](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone.0358568.ref001)]. One of the key mechanisms involved in regulating proteostasis is the ubiquitin-proteasome system (UPS), a multi-component system that relies on the E1-E2-E3 ubiquitin conjugation cascade to selectively mark unwanted proteins for degradation by the proteasome [[1](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone.0358568.ref001),[2](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone.0358568.ref002)]. The largest family of E3 complexes are the Cullin-RING ubiquitin ligases, where a Cullin acts as a scaffold for a RING to transfer ubiquitin from a ubiquitin-carrying E2 to a substrate protein [[2](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone.0358568.ref002)]. However, Cullins require NEDD8 neddylation to maintain the flexibility needed to bring the RING-E2 closer to the substrate protein, thereby enabling efficient transfer of ubiquitin to the substrate protein [[2](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone.0358568.ref002)]. A critical modulator of the UPS process is the highly conserved hetero-octameric protein complex, the COP9 signalosome [[3](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone.0358568.ref003)]. The COP9 signalosome acts as an isopeptidase for NEDD8, fine-tuning Cullin-RING ubiquitin ligase activity and substrate specificity for ubiquitination and subsequent degradation [[3](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone.0358568.ref003)]. A growing body of evidence indicates a COP9 subunit-specific involvement in regulating either oncogenic or tumor suppressor programs in a cancer-dependent manner (reviewed in [[4](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone.0358568.ref004)]). For example, CSN1 was found to contribute to hepatocellular carcinoma migration and proliferation by upregulating cyclinA2 expression [[5](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone.0358568.ref005)]. However, CSN1 was also suggested to act as a tumor suppressor in penile squamous cell carcinoma as CSN1 mutations disrupted miRNA-mediated gene silencing, contributing to disease development [[6](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone.0358568.ref006)]. The variability in cellular programs regulated by the COP9 signalosome in different cancers highlights the need to unbiasedly dissect the involvement, and importance, of each subunit in different cancer types. CSN6 is the only COP9 subunit investigated in glioblastoma, where it was shown to drive tumor cell proliferation by stabilizing the mitogen receptor EGFR [[7](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone.0358568.ref007)]. However, despite the therapeutic interest in targeting the UPS in glioblastoma, the contribution of the other COP9 signalosome subunits within this process remains poorly understood. In this study, we investigated the essentiality of COP9 signalosome subunits for glioblastoma stem cell (GSC) growth _in vitro_. We show that, alongside CSN6 whose role has been previously investigated [[7](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone.0358568.ref007)], CSN1 is also essential for GSC growth _in vitro._ We demonstrate that CSN1 regulates transcriptional profiles associated with the activation of the AP-1 transcription factor and cell cycle progression. Furthermore, we provide the first evidence that CSN1 regulates GSC-driven tumor growth. ## Results ### The COP9 signalosome subunit, CSN1, is essential in GSCs The COP9 signalosome is composed of 8 subunits (CSN1, CSN2, CSN3, CSN4, CSN5, CSN6, CSN7A/7B, and CSN8) [[8](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone.0358568.ref008)] which are encoded by _GPS1, COPS2, COPS3, COPS4, COPS5, COPS6, COPS7A/7B,_ and _COPS8_ , respectively. To identify the most critical subunit in GSCs, we analyzed a previously published genome-wide essentiality screen that encompassed 11 GSCs [[9](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone.0358568.ref009)]. Interestingly, knockout of only two COP9 signalosome subunit genes, _GPS1_ and _COPS6_ , which encode CSN1 and CSN6, respectively, conferred a fitness defect in all 11 GSC cultures ([Fig 1A](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone-0358568-g001)). Given that the role of CSN6 in glioblastoma has been previously investigated [[7](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone.0358568.ref007)], our current study focused on elucidating the contributions of CSN1 to the disease. CSN1 expression was subsequently assessed across a diverse panel of GSC cultures to confirm its broad expression ([Fig 1B](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone-0358568-g001)). [![thumbnail](https://journals.plos.org/plosone/article/figure/image?size=inline&id=10.1371/journal.pone.0358568.g001)](https://journals.plos.org/plosone/article/figure/image?size=medium&id=10.1371/journal.pone.0358568.g001 "Click for larger image") Download: * [PNG larger image](https://journals.plos.org/plosone/article/figure/image?download&size=large&id=10.1371/journal.pone.0358568.g001) * [TIFF original image](https://journals.plos.org/plosone/article/figure/image?download&size=original&id=10.1371/journal.pone.0358568.g001) Fig 1. CSN1 and CSN6 are the most essential COP9 subunits in GSCs. **(A)** Heatmap displaying the Bayes factor essentiality score of genes encoding COP9 signalosome complex subunits in 11 GSC cultures. **(B)** CSN1 protein expression in 7 patient-derived GSC cultures. [ https://doi.org/10.1371/journal.pone.0358568.g001](https://doi.org/10.1371/journal.pone.0358568.g001) ### Loss of CSN1 stunts GSC growth and stemness _in vitro_ and prolongs survival in orthotopic glioblastoma xenograft models To elucidate the functional contributions of CSN1 in GSCs, we performed CRISPR-Cas9 mediated knockout of _GPS1_ , which encodes CSN1, with three gRNAs in two different patient-derived GSC cultures ([Fig 2A](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone-0358568-g002)). This generated stable GSCs with ~20% residual CSN1 expression (GPS1–1) and a near complete knockout of CSN1 (GPS1–2), relative to the AAVS1 control ([Fig 2A](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone-0358568-g002)). We investigated the effect of CSN1 loss on GSC growth by tracking the growth rate of GPS1–1 and GPS1–2 compared to AAVS1 over a 14-day time course ([Fig 2B](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone-0358568-g002)). Results showed that reduced CSN1 expression due to CRISPR-Cas9 targeting significantly inhibited GSC growth over time ([Fig 2B](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone-0358568-g002)-[D](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone-0358568-g002)). Since GSCs targeted with the second _GPS1_ gRNA (GPS1–2) displayed the highest CSN1 knockout efficiency, we utilized them for all remaining experiments in the study and referred to them as CSN1-KO. We then validated the effect of CSN1 on GSC growth by performing EdU flow cytometric analysis. This revealed that CSN1-KO disrupts normal cell cycle progression, displaying a reduced percentage of cells in S and G2 + M phases while accumulating cells in G0/G1 phase relative to the AAVS1 control ([Fig 2E](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone-0358568-g002)-[G](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone-0358568-g002)). We next performed a limiting dilution assay on AAVS1 and CSN1-KO GSCs to determine whether CSN1 regulates GSC stemness. This revealed that CSN1-KO significantly reduced GSC sphere-initiating frequency, correlating with a dramatic reduction in the GSC stemness marker, SOX2 ([Fig 2H](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone-0358568-g002)-[I](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone-0358568-g002)). To determine whether the _in vitro_ growth and stemness defects translated _in vivo,_ we orthotopically xenografted two independent AAVS1 and CSN1-KO GSC cultures into SCID mice. Strikingly, we observed that mice xenografted with CSN1-KO GSCs exhibited a significant survival advantage relative to AAVS1 GSCs ([Fig 2J](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone-0358568-g002)-[K](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0358568#pone-0358568-g002)). [![thumbnail](https://journals.plos.org/plosone/article/figure/image?size=inline&id=10.1371/journal.pone.0358568.g002)](https://journals.plos.org/plosone/article/figure/image?size=medium&id=10.1371/journal.pone.0358568.g002 "Click for larger image") Download: * [PNG larger image](https://journals.plos.org/plosone/article/figure/image?download&size=large&id=10.1371/journal.pone.0358568.g002) * [TIFF original image](https://journals.plos.org/plosone/article/figure/image?download&size=original&id=10.1371/journal.pone.0358568.g002) Fig 2. CSN1 promotes GSC growth and tumorigenesis. **(A)** Western blot validation of CSN1 knockout in BT67 (n = 3) and BT48 (n = 3). **(B)** Growth curves of AAVS1, G
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