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

机译:特异性阻断脂肪酸合成以抑制膀胱癌的恶性表型

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摘要

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:脂肪酸的合成受转录因子SREBPs及其伴游蛋白SCAP的调控。恶性细胞变得依赖于从头脂肪形成,该脂肪形成维持快速的增殖和对细胞应激的抗性。越来越多的证据表明SCAP参与了包括恶性肿瘤在内的各种疾病过程,这些过程调节转录因子SREBPs肿瘤发生与葡萄糖摄入和脂肪形成有关。在我们的研究中,我们发现SCAP在BC组织中上调。 CRISPR-Cas9对SCAP的抑制作用抑制细胞增殖,侵袭和迁移。另外,促进了细胞凋亡。而且,SCAP的下调可能会削弱雌激素对BC的促癌作用。我们的研究表明,SCAP在BC中起着致癌作用,脂肪形成可能通过诱导SCAP促进BC的起始。因此,靶向SCAP可能为治疗BC提供有希望的手段,并为膀胱癌的发生提供新的视角。

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