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首页> 外文期刊>Journal of experimental & clinical cancer research : >HMGA1-TRIP13 axis promotes stemness and epithelial mesenchymal transition of perihilar cholangiocarcinoma in a positive feedback loop dependent on c-Myc
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HMGA1-TRIP13 axis promotes stemness and epithelial mesenchymal transition of perihilar cholangiocarcinoma in a positive feedback loop dependent on c-Myc

机译：HMGA1-TRIP13轴促进依赖于C-MYC的阳性反馈回路中Periwivili胆管癌的茎秆和上皮间充质转变

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Cholangiocarcinoma is a highly malignant cancer with very dismal prognosis. Perihilar cholangiocarcinoma(pCCA) accounts for more than 50% of all cholangiocarcinoma and is well-characterized for its low rate of radical resection. Effects of radiotherapy and chemotherapy of pCCA are very limited. Here we screened potential biomarkers of pCCA with transcriptome sequencing and evaluated the prognostic significance of HMGA1 in a large cohort pCCA consisting of 106 patients. With bioinformatics and in vitro/vivo experiments, we showed that HMGA1 induced tumor cell stemness and epithelial-mesenchymal-transition (EMT), and thus facilitated proliferation, migration and invasion by promoting TRIP13 transcription. Moreover, TRIP13 was also an unfavorable prognostic biomarker of pCCA, and double high expression of HMGA1/TRIP13 could predict prognosis more sensitively. TRIP13 promoted pCCA progression by suppressing FBXW7 transcription and stabilizing c-Myc. c-Myc in turn induced the transcription and expression of both HMGA1 and TRIP13, indicating that HMGA-TRIP13 axis facilitated pCCA stemness and EMT in a positive feedback pathway. HMGA1 and TRIP13 were unfavorable prognostic biomarkers of pCCA. HMGA1 enhanced pCCA proliferation, migration, invasion, stemness and EMT, by inducing TRIP13 expression, suppressing FBXW7 expression and stabilizing c-Myc. Moreover, c-Myc can induce the transcription of HMGA1 and TRIP13, suggesting that HMGA-TRIP13 axis promoted EMT and stemness in a positive feedback pathway dependent on c-Myc.
机译：胆管癌是一种高度恶性癌症，预后非常令人沮丧。 PeriwillionCocarcinoma（PCCA）占所有胆管癌的50％以上，并且具有良好的特征，其根治性切除率低。放射治疗和化疗PCCA的影响非常有限。在这里，我们通过转录组测序筛选PCCA的潜在生物标志物，并评估HMGA1在由106名患者组成的大型队列PCCA中的预后意义。通过生物信息学和体外/体内实验，我们表明HMGA1诱导肿瘤细胞茎和上皮 - 间充质转换（EMT），从而通过促进TRIP13转录，促进增殖，迁移和侵袭。此外，TRIP13也是PCCA的不利预后生物标志物，HMGA1 / TRIP13的双高表达可以预测更灵敏的预后。通过抑制FBXW7转录和稳定C-MYC来推进PCCA进展。 C-MYC反过来诱导HMGA1和TRIP13的转录和表达，表明HMGA-TRIP13轴促进了阳性反馈途径中的PCCA茎和EMT。 HMGA1和TRIP13是PCCA不利的预后生物标志物。通过诱导TRIP13表达，抑制FBXW7表达和稳定C-MYC，增强了PCCA增殖，迁移，侵袭，茎和EMT，抑制了C-MYC。此外，C-MYC可以诱导HMGA1和TRIP13的转录，表明HMGA-TREP13轴促进依赖于C-MYC的正反馈途径中的EMT和茎。

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