ArticleJournal of cellular biochemistry2025
Transforming Growth Factor-β Modulates Cancer Stem Cell Traits on CD44 Subpopulations in Hepatocellular Carcinoma.
Article in Journal of cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed.
- Stemness CD24 activation promotes hepatocellular carcinoma progressionWorld journal of gastroenterology · 2026Article
- Article
- Investigating the role of the TGF-β-SLC20A1 axis in the spatial heterogeneity of hepatocellular carcinoma through single-cell and spatial transcriptomics.Frontiers in immunology · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is a formidable malignancy, with growing interest in identifying cancer stem cells (CSCs) as potential therapeutic targets. CD44 isoforms have emerged as promising CSC markers in HCC, often associated with epithelial-mesenchymal transition (EMT) induced by transforming growth factor-beta (TGF-β). However, the intricate relationship between CSC traits, CD44 isoforms, and TGF-β effects on CD44 subpopulations in HCC remains unclear. This study aimed to clarify how TGF-β influences proteomic changes and CSC traits in subpopulations expressing standard CD44 isoform (CD44std) and CD44 variant 9 (CD44v9). Treating SNU-423 cells with TGF-β lead to notable morphological changes, resembling a spindle-like phenotype, along with reductions in CD44v9+ subpopulations and differential CD44std expression. Proteomic analysis highlighted significant alterations in signaling pathways, particularly the mitogen-activated protein kinase (MAPK) pathway. Validation experiments demonstrated upregulation in CD44std cells and downregulation in CD44v9 cells post-TGF-β treatment. Furthermore, TGF-β exerted regulatory influence over Sox2 and Nanog expression, resulting in increased colony and spheroid formation in CD44std cells but decreased capabilities in CD44v9 cells. TGF-β also enhanced the migratory and invasive properties of both subpopulations through EMT, alongside increased adhesive abilities in CD44v9 cells. These findings illuminate the dynamic interplay between TGF-β and CD44std/CD44v9 subpopulations, emphasizing the role of MAPK signaling and modulation of CSC traits. This research contributes to understanding the dynamic interplay between CD44 isoforms and TGF-β in HCC.
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