Abstract
Epithelial Protein Lost In Neoplasm (EPLIN), also known as LIMA1 (LIM Domain And Actin Binding 1), was first discovered as a protein differentially expressed in normal and cancerous cell lines. It is now known to be key to the progression and metastasis of certain solid tumours. Despite a slow pace in understanding the biological role in cells and body systems, as well as its clinical implications in the early years since its discovery, recent years have witnessed a rapid progress in understanding the mechanisms of this protein in cells, diseases and indeed the body. EPLIN has drawn more attention over the past few years with its roles expanding from cell migration and cytoskeletal dynamics, to cell cycle, gene regulation, angiogenesis/lymphangiogenesis and lipid metabolism. This concise review summarises and discusses the recent progress in understanding EPLIN in biological processes and its implications in cancer.
Highlights
Paxillin–Plectin–Epithelial Protein Lost In Neoplasm (EPLIN) Complex Promotes Apical ExtrusionEPLIN has been indicated in the process of cytokinesis, in which loss of EPLIN and its interacting partners could lead to multinucleation which, in turn, may contribute to carcinogenesis [12,13]
Cardiff China Medical Research Collaborative (CCMRC), Division of Cancer and Genetics (DCG), Abstract: Epithelial Protein Lost In Neoplasm (EPLIN), known as LIMA1
EPLIN has drawn increased attention over the past few years, with its roles expanding from those initially indicated in cell migration and cytoskeletal dynamics to cell cycle, gene regulation, angiogenesis/lymphangiogenesis and lipid metabolism
Summary
EPLIN has been indicated in the process of cytokinesis, in which loss of EPLIN and its interacting partners could lead to multinucleation which, in turn, may contribute to carcinogenesis [12,13]. Its impact on cellular functions in prostate cancer cells may be achieved through regulation of FAK/Src signalling pathways, adding insights to the potential mechanism behind this tumour suppressor Both control and EPLIN-knockdown cell lines, while invasion and migration abilities were only significantly reduced in EPLIN-knockdown CA-HPV-10 cells following FAK. Depleted or mutant EPLIN impacts the interactions with NPC1L1 to weaken cholesterol absorption in intestines, potentially decreasing the risk of high LDL-C-related diseases, which provides a different picture of this tumour suppressor, as its downregulation in cancer cells often leads to promotion of cancer developments. The authors suggested that enhanced EPLIN-α results in elevated binding to the Arp2/3 complex and JAIL formation termination, potentially impacting VE-cadherin dynamics Consistent with this, they demonstrated altered VE-cadherin dynamics in EPLIN-α overexpression HUVEC cells, observing intracellular gaps and disrupted VE-cadherin at cell contacts, together with decreased migration and barrier function [42].
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