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Specifically blocking the fatty acid synthesis to inhibit the malignant phenotype of bladder cancer

机译:特别是阻断脂肪酸合成以抑制膀胱癌的恶性表型

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Fatty acid synthesis is regulated by transcription factors SREBPs and their escort protein SCAP. Malignant cells become dependent on de novo lipogenesis, which sustains rapid proliferation and resistance to cellular stress. Increasing evidence showed SCAP participated in various disease processes including malignant tumors, which regulate transcription factors SREBPs Tumorigenesis is associated with incur glucose consumption and lipogenesis. In our study, we discovered that SCAP was upregulated in BC tissues. SCAP knockdown by CRISPR-Cas9 inhibit the cell proliferation, invasion and migration. Additionally, the cell apoptosis was facilitated. What's more, downregulation of SCAP could weaken the cancer-promoting effects of estrogen on BC. Our study revealed that SCAP played a carcinogenic role in BC and lipogenesis might promote the initiation of BC by inducing SCAP. Thus, Targeting SCAP may provide a promising means of treating BC and a new perspective for the tumorigenesis of bladder cancer.
机译:脂肪酸合成由转录因子Srebps及其护送蛋白质碎片调节。恶性细胞变得依赖于Novo脂肪生成,其维持快速增殖和对细胞胁迫的抗性。越来越多的证据表明,SCAP参与了各种疾病过程,包括恶性肿瘤,调节转录因子Srebps肿瘤发生与血糖消耗和脂肪生成有关。在我们的研究中,我们发现在BC组织中被上调了SCAP。 CRISPR-CAS9的SCAP敲低抑制细胞增殖,入侵和迁移。另外,促进了细胞凋亡。更重要的是,突出的下调可能会削弱雌激素对BC的癌症促进作用。我们的研究表明,突然在BC和脂肪生成中发挥了致癌作用,可以通过诱导液体来促进BC的启动。因此,靶向SCAP可以提供治疗BC的有希望的方法和膀胱癌的肿瘤鉴定的新视角。

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