ArticleAmerican journal of translational research2023
KCTD10 functions as a tumor suppressor in hepatocellular carcinoma by triggering the Notch signaling pathway.
Article in American journal of translational research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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
5 citing papers in PubMed.
- Current research of the Notch pathway in hepatocellular carcinoma.European journal of medical research · 2025Review
- VPS45 Contributes to the Progression of Hepatocellular Carcinoma by Triggering the Wnt/β-Catenin Signaling Pathway.Molecular carcinogenesis · 2025Article
- Elucidating the role of KCTD10 in coronary atherosclerosis: Harnessing bioinformatics and machine learning to advance understanding.Scientific reports · 2025Article
- KCTD10 inhibits lung cancer metastasis and angiogenesis via ubiquitin-mediated β-catenin degradation.Frontiers in immunology · 2025Article
- The CRL3Proceedings of the National Academy of Sciences of the United States of America · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveOur previous study found KCTD10 negatively regulates Notch signaling, but whether KCTD10 regulates human hepatocellular carcinoma (HCC) carcinogenicity was uncertain.
methodsWe used lentivirus infection to regulate KCTD10 expression in HCC cell lines, then monitored tumor sphere formation rate, cell migration,
resultsDown-regulation of KCTD10 in HCC cell lines (Hep3B and MHCC97H) enhanced the expression of CSC marker genes, promoted self-renewal and tumorigenic ability, and increased the CD133
conclusionsThe results demonstrated that KCTD10 can act as a tumor suppressor in HCC cells through Notch signaling.
Indexed as
Identifiers
36777839PMC9908486What OpenQuestion holds
Registered trials
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