ArticleMolecular medicine reports2021
CSN1 facilitates proliferation and migration of hepatocellular carcinoma cells by upregulating cyclin A2 expression.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
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- Differential roles of cyclin-CDK1 complexes in cell migration and invasion.Journal of cell science · 2025Article
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- DNA copy number profiles and systems biology connect chromatin remodeling and DNA repair in high-risk neuroblastoma.Genetics and molecular biology · 2024Article
- Integrated proteome and phosphoproteome analysis of gastric adenocarcinoma reveals molecular signatures capable of stratifying patient outcome.Molecular oncology · 2023Article
- Mammaglobin 1 mediates progression of trastuzumab-resistant breast cancer cells through regulation of cyclins and NF-κB.FEBS open bio · 2022Article
- Article
- miR‑374c‑5p regulates PTTG1 and inhibits cell growth and metastasis in hepatocellular carcinoma by regulating epithelial‑mesenchymal transition.Molecular medicine reports · 2022Article
- Article
- Screening of Hub Genes in Hepatocellular Carcinoma Based on Network Analysis and Machine Learning.Computational and mathematical methods in medicine · 2022Article
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Authors and funding
5 authors at 2 institutions in 1 country.
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Abstract
Constitutive photomorphogenesis 9 signalosome subunit 1 (CSN1) plays an important role in the ubiquitin-proteasome pathway and regulates various cellular processes, such as the cell cycle and DNA repair. The CSN complex consists of eight subunits (CSN1 to CSN8) and regulates the tumorigenesis of a variety of tumor types. However, the exact role of CSN1 in hepatocellular carcinoma (HCC) remains unclear. The present study evaluated the expression and biological effects of CSN1 in HCC tissue samples and cell lines. CSN1 was significantly overexpressed in HCC tissue and cell lines, compared with their normal counterparts. In patients with HCC, elevated CSN1 levels correlated with tumor size, tumor metastasis and tumor stage. Loss‑of‑function assays indicated that CSN1 knockdown inhibited the proliferation and migration HCC cells. In addition, CSN1 promoted the expression of cyclin A2 in a ubiquitination‑independent manner. Lastly, xenograft experiments indicated that CSN1 promoted HCC tumor growth <em>in vivo</em>. The present study suggested that CSN1 inhibition could represent a potential approach for the prevention of HCC progression and metastasis.
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