The Roles of Tricellular Tight Junction Protein Angulin-1/Lipolysis-Stimulated Lipoprotein Receptor (LSR) in Endometriosis and Endometrioid-Endometrial Carcinoma.
The Roles of Tricellular Tight Junction Protein Angulin-1/Lipolysis-Stimulated Lipoprotein Receptor (LSR) in Endometriosis and Endometrioid-Endometrial Carcinoma.
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DOI：
10.3390/cancers13246341
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发表时间：
2021-12-17
期刊：
影响因子：
5.2
通讯作者：
Kojima T
中科院分区：
文献类型：
--
作者：
Shimada H;Kohno T;Konno T;Okada T;Saito K;Shindo Y;Kikuchi S;Tsujiwaki M;Ogawa M;Matsuura M;Saito T;Kojima T
紧密连接蛋白的异常与上皮-间质转化（EMT）和多种肿瘤的恶性程度密切相关。Angulin-1/Lipolysis-stimulated lipoprotein receptor（LSR）是一种新型的三细胞接触分子，具有屏障功能。angulin-1/LSR的缺失与多种癌症中的恶性程度相关，包括子宫内膜样癌（EEC）。此外，在人EEC细胞系Sawano中，在三细胞接触处，angulin-1/LSR的缺失上调claudin-1，并且刺激凋亡的p53蛋白2（ASPP 2）的缺失下调angulin-1/LSR。Angulin-1/LSR和ASPP 2在Sawano胞质分裂过程中集中在中间体和中心体。在EEC组织中，在恶性肿瘤期间，angulin-1/LSR和ASPP 2减少，claudin-2过表达，而在子宫内膜异位症组织中，观察到angulin-1/LSR和claudin-2的定位变化。本文综述了angulin-1/LSR的缺失如何促进子宫内膜异位症和EEC的进展，并讨论了通过多种信号通路及其相关蛋白治疗angulin-1/LSR的可能性。紧密连接蛋白在细胞通透性屏障功能之外发挥作用，控制细胞增殖和分化。紧密连接与信号转导通路的关系影响细胞的生长、侵袭和迁移。紧密连接蛋白的异常与上皮间质转化（EMT）和多种肿瘤的恶性程度密切相关。Angulin-1/脂解刺激的脂蛋白受体（LSR）形成具有屏障功能的三细胞接触。angulin-1/LSR的下调与各种癌症的恶性程度相关，包括子宫内膜样-子宫内膜癌（EEC）。这些改变不仅与多种信号通路如Hippo/雅普、HDAC、AMPK有关，而且与ECC细胞系Sawano中的细胞代谢有关。此外，缺失angulin-1/LSR上调claudin-1，缺失凋亡刺激p53蛋白2（ASPP 2）下调angulin-1/LSR。Angulin-1/LSR和ASPP 2在胞质分裂过程中均集中于中间体和中心体。在EEC组织中，在恶性肿瘤期间，angulin-1/LSR和ASPP 2减少，claudin-2过表达，而在子宫内膜异位症组织中，观察到angulin-1/LSR和claudin-2的定位变化。本文综述了angulin-1/LSR下调如何促进子宫内膜异位症和EEC的发生发展，并讨论了angulin-1/LSR及其相关蛋白，包括claudins和ASPP 2的作用。
Abnormality of tight junction proteins closely contributes to epithelial–mesenchymal transition (EMT) and the malignancy of various cancers. Angulin-1/lipolysis-stimulated lipoprotein receptor (LSR) is a novel molecular constituent of tricellular contacts that has a barrier function. Loss of angulin-1/LSR correlates with the malignancy in various cancers, including endometrioid-endometrial carcinoma (EEC). Moreover, loss of angulin-1/LSR upregulates claudin-1, and loss of apoptosis-stimulating p53 protein 2 (ASPP2) at tricellular contacts downregulates angulin-1/LSR in human EEC cell line Sawano. Angulin-1/LSR and ASPP2 concentrate at both midbody and centrosome during cytokinesis in Sawano. In EEC tissues, angulin-1/LSR and ASPP2 are reduced and claudin-2 is overexpressed during malignancy, while in the tissues of endometriosis changes in localization of angulin-1/LSR and claudin-2 are seen. This review highlights how the loss of angulin-1/LSR promotes the progression of endometriosis and EEC and discusses the possibility of therapeutic targeting for angulin-1/LSR via multiple signaling pathways and its related proteins. Tight junction proteins play roles beyond permeability barriers functions and control cell proliferation and differentiation. The relation between tight junctions and the signal transduction pathways affects cell growth, invasion and migration. Abnormality of tight junction proteins closely contributes to epithelial mesenchymal transition (EMT) and malignancy of various cancers. Angulin-1/lipolysis-stimulated lipoprotein receptor (LSR) forms tricellular contacts that has a barrier function. Downregulation of angulin-1/LSR correlates with the malignancy in various cancers, including endometrioid-endometrial carcinoma (EEC). These alterations have been shown to link to not only multiple signaling pathways such as Hippo/YAP, HDAC, AMPK, but also cell metabolism in ECC cell line Sawano. Moreover, loss of angulin-1/LSR upregulates claudin-1, and loss of apoptosis stimulating p53 protein 2 (ASPP2) downregulates angulin-1/LSR. Angulin-1/LSR and ASPP2 concentrate at both midbody and centrosome in cytokinesis. In EEC tissues, angulin-1/LSR and ASPP2 are reduced and claudin-2 is overexpressed during malignancy, while in the tissues of endometriosis changes in localization of angulin-1/LSR and claudin-2 are seen. This review highlights how downregulation of angulin-1/LSR promotes development of endometriosis and EEC and discusses about the roles of angulin-1/LSR and its related proteins, including claudins and ASPP2.
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