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首页> 外文期刊>Anticancer Research: International Journal of Cancer Research and Treatment >GLI1 and CTNNB1 Knockdown Activates NOTCH and mTOR Signalling in NB4 Myeloid Leukaemia Cells
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GLI1 and CTNNB1 Knockdown Activates NOTCH and mTOR Signalling in NB4 Myeloid Leukaemia Cells

机译：GLI1和CTNNB1敲击在NB4骨髓白血病细胞中激活NOTCH和MTOR信号传导

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Background: Hedgehog (HH), WNT, NOTCH, and mechanistic target of rapamycin (mTOR) signalling pathways are known to regulate the progression of cancer; however, their interaction in leukaemia cells is not fully clarified. Materials and Methods: Myeloid and T-lymphoblastic leukaemia cell lines (NB4, THP-1, Jurkat, and DND-41) were transfected with small interfering RNAs targeting the glioma-associated oncogene homolog 1 (GLI1) and catenin beta-1 (CTNNB1) genes involved in the regulation of HH and WNT pathways, respectively, and we examined cell proliferation and gene expression. Results: The knockdown of GM and CTNNB1 did not significantly affect proliferation of any cell line; however, it up-regulated the expression of NOTCH1, cleaved NOTCH1 fragment, and phosphorylated mTOR in NB4 cells, but not in the other cell lines. Conclusion: Our data suggest that HH and WNT act upstream of NOTCH and mTOR pathways and negatively regulate them in myeloid NB4 cells. Further studies are required to determine the biological significance of this signalling crosstalk in leukaemia.
机译：背景：哈奇霍（HH），WNT，凹口和雷帕霉素（MTOR）信号传导途径的机械靶标明调节癌症的进展;然而，它们在白血病细胞中的相互作用并未完全澄清。材料和方法：用靶向胶质瘤相关的癌基因同源物1（GLI1）和Catenin Beta-1的小干扰RNA（CTNNB1分别参与HH和WNT途径调节的基因，并检查了细胞增殖和基因表达。结果：GM和CTNNB1的敲低没有显着影响任何细胞系的增殖;然而，它上调Notch1，切割的Notch1片段和磷酸化MTOR在NB4细胞中的表达，但不在其他细胞系中。结论：我们的数据表明，HH和WNT在凹口和MTOR途径上游作用，并在骨髓NB4细胞中负面调节它们。需要进一步的研究来确定白血病中该信号串扰的生物学意义。

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