Novel insights into the roles of migrasome in cancer

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Abstract

Cell migration, a hallmark of cancer malignancy, plays a critical role in cancers. Improperly initiated or misdirected cell migration can lead to invasive metastatic cancer. Migrasomes are newly discovered vesicular cellular organelles produced by migrating cells and depending on cell migration. Four marker proteins [NDST1 (bifunctionalheparan sulfate N-deacetylase/N-sulfotransferase 1), EOGT (Epidermal growth factor domains pecific O-linked N-acetylglucosaminetransferase), CPQ (carboxypeptidase Q), and PIGK (phosphatidylinositol glycan anchor biosynthesis, class K)] of migrasomes were successfully identified. There are three marker proteins (NDST1, PIGK, and EOGT) of migrasome expressed in cancer. In this review, we will discuss the process of migrasome discovery, the formation of migrasome, the possible functions of migrasome, and the differences between migrasomes and exosomes, especially, the biological functions of migrasome marker proteins in cancer, and discuss some possible roles of migrasomes in cancer. We speculate that migrasomes and migracytosis can play key roles in regulating the development of cancer.

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Most cited references 86

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Exosomes

D Pegtel, Stephen Gould (2019)

Exosomes are small, single-membrane, secreted organelles of ∼30 to ∼200 nm in diameter that have the same topology as the cell and are enriched in selected proteins, lipids, nucleic acids, and glycoconjugates. Exosomes contain an array of membrane-associated, high-order oligomeric protein complexes, display pronounced molecular heterogeneity, and are created by budding at both plasma and endosome membranes. Exosome biogenesis is a mechanism of protein quality control, and once released, exosomes have activities as diverse as remodeling the extracellular matrix and transmitting signals and molecules to other cells. This pathway of intercellular vesicle traffic plays important roles in many aspects of human health and disease, including development, immunity, tissue homeostasis, cancer, and neurodegenerative diseases. In addition, viruses co-opt exosome biogenesis pathways both for assembling infectious particles and for establishing host permissiveness. On the basis of these and other properties, exosomes are being developed as therapeutic agents in multiple disease models.

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Exosomes Facilitate Therapeutic Targeting of Oncogenic Kras in Pancreatic Cancer

Sushrut Kamerkar, Valerie LeBleu, Hikaru Sugimoto … (2017)

Summary The mutant form of the GTPase KRAS is a key driver of pancreatic cancer but remains a challenging therapeutic target. Exosomes, extracellular vesicles generated by all cells, are naturally present in the blood. Here we demonstrate that enhanced retention of exosomes in circulation, compared to liposomes, is due to CD47 mediated protection of exosomes from phagocytosis by monocytes and macrophages. Exosomes derived from normal fibroblast-like mesenchymal cells were engineered to carry siRNA or shRNA specific to oncogenic KRASG12D (iExosomes), a common mutation in pancreatic cancer. Compared to liposomes, iExosomes target oncogenic Kras with an enhanced efficacy that is dependent on CD47, and is facilitated by macropinocytosis. iExosomes treatment suppressed cancer in multiple mouse models of pancreatic cancer and significantly increased their overall survival. Our results inform on a novel approach for direct and specific targeting of oncogenic Kras in tumors using iExosomes.

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Non-muscle myosin II takes centre stage in cell adhesion and migration.

Miguel Vicente-Manzanares, Xuefei Ma, Robert S Adelstein … (2009)

Non-muscle myosin II (NM II) is an actin-binding protein that has actin cross-linking and contractile properties and is regulated by the phosphorylation of its light and heavy chains. The three mammalian NM II isoforms have both overlapping and unique properties. Owing to its position downstream of convergent signalling pathways, NM II is central in the control of cell adhesion, cell migration and tissue architecture. Recent insight into the role of NM II in these processes has been gained from loss-of-function and mutant approaches, methods that quantitatively measure actin and adhesion dynamics and the discovery of NM II mutations that cause monogenic diseases.

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Author and article information

Contributors

Xiaoyan Yang: yyangxiaoyan@163.com

Journal

Journal ID (nlm-ta): Discov Oncol

Journal ID (iso-abbrev): Discov Oncol

Title: Discover Oncology

Publisher: Springer US (New York )

ISSN (Electronic): 2730-6011

Publication date (Electronic): 15 May 2024

Publication date PMC-release: 15 May 2024

Publication date Collection: December 2024

Volume: 15

Electronic Location Identifier: 166

Affiliations

School of Pharmaceutical Science, Hengyang Medical College, University of South China, ( https://ror.org/03mqfn238) 28 Western Changsheng Road, Hengyang , 421001 Hunan, People’s Republic of China

Article

Publisher ID: 942

DOI: 10.1007/s12672-024-00942-0

PMC ID: 11096295

PubMed ID: 38748047

SO-VID: 409a1837-64e0-4d6b-a5bb-f61b20a4a11b

License:

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

History

Date received : 14 October 2023

Date accepted : 18 March 2024

Funding

Funded by: Postgraduate Research Innovation Project of Hunan Province

Award ID: CX20221028

Award Recipient : Yiwen Wu

Custom metadata

Keywords: cell migration,cancer,migrasome,specific marker proteins of migrasome,migracytosis

Data availability:

Keywords: cell migration, cancer, migrasome, specific marker proteins of migrasome, migracytosis

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