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首页> 外文期刊>World Journal of Gastroenterology >Signaling pathway of insulin-like growth factor-II as a target of molecular therapy for hepatoblastoma.
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Signaling pathway of insulin-like growth factor-II as a target of molecular therapy for hepatoblastoma.

机译：胰岛素样生长因子-II作为肝母细胞瘤分子治疗靶标的信号通路。

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AIM: To 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. METHODS: Huh-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. RESULTS: IGF-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 numberto 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. CONCLUSION: IGF-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.
机译：目的：探讨胰岛素样生长因子（IGF）-II是一种生长因子及其信号传导途径的可能性，以开发针对肝母细胞瘤的分子疗法。方法：使用人类肝母细胞瘤细胞株Huh-6和HepG2。将IGF-II添加到缺乏血清的培养基中。进行蛋白质印迹分析以阐明IGF-1受体（IGF-1R）的表达。添加了IGF-1R（鬼臼苦素，PPP），磷脂酰肌醇（PI）3-激酶（LY294002和Wortmannin）或促分裂原活化蛋白（MAP）激酶（PD98059）的抑制剂以揭示IGF-II的信号传导途径。用苏木精-伊红染色对细胞进行形态学分析，以揭示其抑制细胞增殖的机制。结果：IGF-II刺激的细胞（HepG2）增殖至2.7（269％+ /-76％）（平均+/- SD）（Huh-6）和2.1（211％+ /-85％）倍。 IGF-1R在Huh-6和HepG2中表达。 PPP将细胞数抑制为44％+ /-11％（Huh-6）和39％+ /-5％（HepG2）。 LY294002和Wortmannin将细胞数抑制为30％+ /-5％（Huh-6），44％+ /-0.4％（HepG2），49％+ /-1.0％（Huh-6）和46％+ /-1.1 ％（HepG2）。 PD98059将HepG2的细胞数抑制为33％+ /-11％，但对Huh-6则没有。禁止细胞增殖时，许多Huh-6和HepG2细胞都死于定向分裂或核分裂，表明细胞凋亡。结论：通过IGF-I受体和PI3激酶证明IGF-II是肝母细胞瘤的生长因子，是分子治疗靶点的良好候选药物。

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