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The roles of FOXM1 in pancreatic stem cells and carcinogenesis

机译：FOXM1在胰腺干细胞和癌变中的作用

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Pancreatic ductal adenocarcinoma (PDAC) has one of the poorest prognoses among all cancers. Over the past several decades, investigators have made great advances in the research of PDAC pathogenesis. Importantly, identification of pancreatic cancer stem cells (PCSCs) in pancreatic cancer cases has increased our understanding of PDAC biology and therapy. PCSCs are responsible for pancreatic tumorigenesis and tumor progression via a number of mechanisms, including extensive proliferation, self-renewal, high tumorigenic ability, high propensity for invasiveness and metastasis, and resistance to conventional treatment. Furthermore, emerging evidence suggests that PCSCs are involved in the malignant transformation of pancreatic intraepithelial neoplasia. The molecular mechanisms that control PCSCs are related to alterations of various signaling pathways, for instance, Hedgehog, Notch, Wnt, B-cell-specific Moloney murine leukemia virus insertion site 1, phosphoinositide 3-kinase/AKT, and Nodal/Activin. Also, authors have reported that the proliferation-specific transcriptional factor Forkhead box protein M1 is involved in PCSC self-renewal and proliferation. In this review, we describe the current knowledge about the signaling pathways related to PCSCs and the early stages of PDAC development, highlighting the pivotal roles of Forkhead box protein M1 in PCSCs and their impacts on the development and progression of pancreatic intraepithelial neoplasia.
机译：胰腺导管腺癌（PDAC）是所有癌症中最差的预后之一。在过去的几十年中，研究人员在PDAC发病机理的研究中取得了长足的进步。重要的是，在胰腺癌病例中鉴定胰腺癌干细胞（PCSC）已增加了我们对PDAC生物学和疗法的了解。 PCSC通过多种机制负责胰腺癌的发生和发展，包括广泛的增殖，自我更新，高致瘤能力，高侵袭性和转移倾向以及对常规治疗的抵抗力。此外，新出现的证据表明PCSCs参与胰腺上皮内瘤变的恶性转化。控制PCSC的分子机制与各种信号通路的改变有关，例如，刺猬，Notch，Wnt，B细胞特异性莫洛尼鼠白血病病毒插入位点1，磷酸肌醇3-激酶/ AKT和Nodal /激活素。此外，作者还报道了增殖特异性转录因子叉头盒蛋白M1参与PCSC的自我更新和增殖。在这篇综述中，我们描述了与PCSCs和PDAC发育早期有关的信号通路的当前知识，强调了PCSCs中叉头盒蛋白M1的关键作用及其对胰腺上皮内瘤变发展和进展的影响。

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