The Roles of Tricellular Tight Junction Protein Angulin-1/Lipolysis-Stimulated Lipoprotein Receptor (LSR) in Endometriosis and Endometrioid-Endometrial Carcinoma

Hiroshi Shimada; Takayuki Kohno; Takumi Konno; Tadahi Okada; Kimihito Saito; Yuma Shindo; Shin Kikuchi; Mitsuhiro Tsujiwaki; Marie Ogawa; Motoki Matsuura; Tsuyoshi Saito; Takashi Kojima

doi:10.3390/cancers13246341

The Roles of Tricellular Tight Junction Protein Angulin-1/Lipolysis-Stimulated Lipoprotein Receptor (LSR) in Endometriosis and Endometrioid-Endometrial Carcinoma

Hiroshi Shimada, Takayuki Kohno, Takumi Konno, Tadahi Okada, Kimihito Saito, Yuma Shindo, Shin Kikuchi, Mitsuhiro Tsujiwaki, Marie Ogawa, Motoki Matsuura, Tsuyoshi Saito, Takashi Kojima

Cancers · 2021 · vol. 13(24) , pp. 6341 · doi:10.3390/cancers13246341 · PMID:34944960 · PMC8699113 · W4200207880

review OA: gold CC0 ⤵ 2 in-corpus citations

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Abstract

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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[1] Activated Hippo/Yes-Associated Protein Pathway Promotes Cell Proliferation and Anti-apoptosis in Endometrial Stromal Cells of Endometriosis 2016

[2] Epithelial-to-Mesenchymal Transition in the Female Reproductive Tract: From Normal Functioning to Disease Pathology 2017

[3] Leptin promotes human endometriotic cell migration and invasion by up-regulating MMP-2 through the JAK2/STAT3 signaling pathway 2015

[4] Direct Cell–Cell Interactions in the Endometrium and in Endometrial Pathophysiology 2018