ArticleCell death discovery2025
CERS6 promotes esophageal squamous cell carcinoma proliferation by increasing the stability of RPN1.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- EGFL6 predicts unfavorable prognosis and serves as a potential indicator in esophageal carcinoma.Discover oncology · 2026Article
- Aloperine Suppresses the Tumorigenicity of Esophageal Squamous Cell Carcinoma by Targeting the AP-1/IL-6/STAT3 Signaling Axis.Biomolecules · 2026Article
- Identification of serum 5'tRF-Val as a promising non-invasive biomarker for early detection of esophageal cancer.Scientific reports · 2026Article
- Gene Expression Analysis of Mitochondria-Associated Membrane (MAM)-Related Genes in ER Stress and Alzheimer's Disease.Cellular and molecular neurobiology · 2026Article
- EpCAM as a novel target of MARCH8: implications for esophageal squamous cell carcinoma progression.Journal of molecular histology · 2026Article
- RPN1 at the crossroads of glycosylation, tumor immunity, and disulfidptosis.Frontiers in pharmacology · 2026Review
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
Esophageal squamous cell carcinoma (ESCC) is associated with poor prognosis because it is typically diagnosed at a moderate or advanced stage. Investigating the precise molecular mechanism of ESCC pathogenesis is essential for developing new therapeutic strategies. In this study, we demonstrated that ceramide synthase 6 (CERS6) was overexpressed and correlated with a worse prognosis in ESCC. Moreover, CERS6 promoted ESCC cell proliferation in vitro and in vivo. Mechanistically, CERS6 sustained the stability of ribophorin 1 (RPN1) by inhibiting its ubiquitination. Subsequently, CERS6 reduced endoplasmic reticulum (ER) stress and reactive oxygen species (ROS) by activating the RPN1-inositol-requiring enzyme 1 (IRE1)-X-box binding protein 1 (XBP1) signaling pathway. Interestingly, the antisense oligonucleotides (ASOs) targeting CERS6 inhibited the growth of ESCC through the RPN1-IRE1-XBP1 signaling pathway. Collectively, our study reveals an unprecedented function and mechanism of CERS6, which is distinct from ceramide synthases, in the development of ESCC, highlighting its potential as a promising therapeutic target.
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Registered trials
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