ArticleWorld journal of gastroenterology2006
Signaling pathway of insulin-like growth factor-II as a target of molecular therapy for hepatoblastoma.
Article in World journal of gastroenterology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 30 citations in OpenAlex.
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- Upregulation of the lncRNACells · 2026Article
- Hepatoblastoma: From Molecular Mechanisms to Therapeutic Strategies.Current oncology (Toronto, Ont.) · 2025Review
- Effect of curcumin on vascular endothelial growth factor in hypoxic HepG2 cells via the insulin-like growth factor 1 receptor signaling pathway.Experimental and therapeutic medicine · 2018Article
- Picropodophyllin and sorafenib synergistically suppress the proliferation and motility of hepatocellular carcinoma cells.Oncology letters · 2014Article
- Current and future management strategies for relapsed or progressive hepatoblastoma.Paediatric drugs · 2012Review
- Regulation of hypoxia-inducible factor-1α (HIF-1α) expression by interleukin-1β (IL-1 β), insulin-like growth factors I (IGF-I) and II (IGF-II) in human osteoarthritic chondrocytes.Clinics (Sao Paulo, Brazil) · 2012Article
- Insulin-like growth factor-I receptor in proliferation and motility of pancreatic cancer.World journal of gastroenterology · 2010Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo address the possibility that insulin-like growth factor (IGF)-II is a growth factor and its signaling pathway so as to develop a molecular therapy for hepatoblastoma.
methodsHuh-6 and HepG2, human hepatoblastoma cell lines, were used. IGF-II was added to the medium deprived of serum. Western blot analysis was performed to clarify the expression of IGF-I receptor (IGF-IR). Inhibitors of IGF-IR (piclopodophyllin, PPP), phosphatidyl-inositol (PI) 3-kinase (LY294002 and Wortmannin), or mitogen-activated protein (MAP) kinase (PD98059) were added to unveil the signaling pathway of IGF-II. Cells were analyzed morphologically with hematoxylin-eosin staining to reveal the mechanism of suppression of cell proliferation.
resultsIGF-II stimulated cells proliferated to 2.7 (269%+/-76%) (mean+/-SD) (Huh-6) and 2.1 (211%+/-85%) times (HepG2). IGF-IR was expressed in Huh-6 and HepG2. PPP suppressed the cell number to 44%+/-11% (Huh-6) and 39%+/-5% (HepG2). LY294002 and Wortmannin suppressed the cell number to 30%+/-5% (Huh-6), 44%+/-0.4% (HepG2), 49%+/-1.0% (Huh-6) and 46%+/-1.1% (HepG2), respectively. PD98059 suppressed the cell number to 33%+/-11% for HepG2 but not for Huh-6. When cell proliferation was prohibited, many Huh-6 and HepG2 cells were dead with pyknotic or fragmented nuclei, suggesting apoptosis.
conclusionIGF-II was shown to be a growth factor of hepatoblastoma via IGF-I receptor and PI3 kinase which were good candidates for target of molecular therapy.
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