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首页> 外文期刊>Oncogene >miR-100 suppresses IGF2 and inhibits breast tumorigenesis by interfering with proliferation and survival signaling
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miR-100 suppresses IGF2 and inhibits breast tumorigenesis by interfering with proliferation and survival signaling

机译：miR-100通过干扰增殖和存活信号传导来抑制IGF2并抑制乳腺肿瘤发生

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Dysregulation of micro RNAs is crucially implicated in tumorigenesis. We detected downregulation of miR-100 in breast cancer cells, leading to an upregulation of the proliferation- and survival-promoting oncogene insulin-like growth factor (IGF) 2 . Stable overexpression of miR-100 strongly reduced IGF2 expression and inhibited tumor growth. In invasive human breast tumors, miR-100 was reduced about fourfold as compared with benign patient samples, whereas IGF2 was strongly enhanced. MiR-100 has also been shown to suppress other proteins of the IGF/mammalian target of rapamycin (mTOR) signaling cascade in different human tumors. Our results reveal miR-100 as a context-dependent master regulator of the IGF/mTOR pathway and a potential target for therapeutic approaches.
机译：微小RNA的失调与肿瘤的发生密切相关。我们在乳腺癌细胞中检测到miR-100的下调，从而导致了增殖和存活促进癌基因胰岛素样生长因子（IGF）2的上调。 miR-100的稳定过表达会大大降低IGF2的表达并抑制肿瘤的生长。在侵袭性人类乳腺肿瘤中，与良性患者样品相比，miR-100减少了约四倍，而IGF2则被大大增强。 MiR-100还显示可抑制不同人类肿瘤中IGF /雷帕霉素哺乳动物靶标（mTOR）信号级联的其他蛋白质。我们的结果表明，miR-100是IGF / mTOR途径的上下文相关主调节剂，是治疗方法的潜在靶标。

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