Restoration of FBP1 suppressed Snail-induced epithelial to mesenchymal transition in hepatocellular carcinoma.
Restoration of FBP1 suppressed Snail-induced epithelial to mesenchymal transition in hepatocellular carcinoma.
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FBP1 的恢复抑制了 Snail 诱导的肝细胞癌上皮细胞向间质细胞的转变。
DOI：
10.1038/s41419-018-1165-x
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发表时间：
2018-11-14
影响因子：
9
通讯作者：
Peng BG
中科院分区：
文献类型：
--
作者：
Liu GM;Li Q;Zhang PF;Shen SL;Xie WX;Chen B;Wu J;Hu WJ;Huang XY;Peng BG
果糖-1,6-二磷酸酶（FBP1）是一种限速糖异生酶，在几种癌症中起着关键作用，并被视为肿瘤抑制因子。然而，其在肝细胞癌（HCC）中的作用尚不清楚。在这里，我们证明了FBP1在蜗牛诱导的肝细胞癌上皮到间充质转化（EMT）和组织中被显著抑制。恢复肝癌细胞中FBP1的表达可抑制SMMC-7721细胞中蜗牛过表达诱导的EMT表型、肿瘤迁移和肿瘤生长。基因集富集分析显示，与低螺和高FBP1组相比，高螺和低FBP1组的WNT、Notch、ESC、CSR和PDGF显著富集。FBP1低表达与AFP升高、卫星结节、门静脉肿瘤血栓、肿瘤分期明显相关。生存分析显示，FBP1是总生存和无复发生存的独立预后因素。总之，我们的研究揭示了FBP1在蜗牛诱导的EMT和HCC预后预测中的重要作用。
Fructose-1,6-bisphosphatase (FBP1), one of the rate-limiting gluconeogenic enzymes, plays critical roles in several cancers and is treated as a tumour suppressor. However, its role in hepatocellular carcinoma (HCC) is unclear. Here, we demonstrated that FBP1 was significantly inhibited during Snail-induced epithelial to mesenchymal transition (EMT) and tissues in HCC. Restoration of FBP1 expression in HCC cancer cells suppressed EMT phenotype, tumour migration and tumour growth induced by Snail overexpression in SMMC-7721 cells. Gene set enrichment analyses revealed significantly enriched terms, including WNT, Notch, ESC, CSR and PDGF, in the group with high Snail and low FBP1 compared with those with low Snail and high FBP1. Low FBP1 expression was significantly correlated with higher AFP level, satellite nodules, portal vein tumour thrombus, and advanced tumour stage. Survival analyses showed that FBP1 was an independent prognostic factor for overall survival and recurrence-free survival. In conclusion, our study revealed a vital role for FBP1 in Snail-induced EMT and prognostic prediction in HCC.
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DOI：
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