Identification of markers for migrasome detection

Zhao, Xiaoxin; Lei, Yaxin; Zheng, Jiajia; Peng, Junya; Li, Ying; Yu, Li; Chen, Yang

doi:10.1038/s41421-019-0093-y

Cited by 81 publications

(109 citation statements)

References 7 publications

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“…It has been recently shown that cells release migrasomes during cell migration from cellular cilia, the tail of the cell [17,191]. The proteome of migrasomes was 27% in common with exosomes, while the remaining 73% was specific to migrasomes [191]. These findings prompted us to hypothesize that EMT-driven migration of cancer cells may promote the release of EVs, which enhances drug ejection and resistance in malignant cells.…”

Section: Exosomal Drug Resistancementioning

confidence: 97%

See 1 more Smart Citation

A Novel Model of Cancer Drug Resistance: Oncosomal Release of Cytotoxic and Antibody-Based Drugs

Eguchi

Taha

Calderwood

et al. 2020

Biology

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Extracellular vesicles (EVs), such as exosomes or oncosomes, often carry oncogenic molecules derived from tumor cells. In addition, accumulating evidence indicates that tumor cells can eject anti-cancer drugs such as chemotherapeutics and targeted drugs within EVs, a novel mechanism of drug resistance. The EV-releasing drug resistance phenotype is often coupled with cellular dedifferentiation and transformation in cells undergoing epithelial-mesenchymal transition (EMT), and the adoption of a cancer stem cell phenotype. The release of EVs is also involved in immunosuppression. Herein, we address different aspects by which EVs modulate the tumor microenvironment to become resistant to anticancer and antibody-based drugs, as well as the concept of the resistance-associated secretory phenotype (RASP).

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Section: Exosomal Drug Resistancementioning

confidence: 97%

“…EMT, almost by definition, enhances the motility and migration of tumor cells. It has been recently shown that cells release migrasomes during cell migration from cellular cilia, the tail of the cell [17,191]. The proteome of migrasomes was 27% in common with exosomes, while the remaining 73% was specific to migrasomes [191].…”

Section: Exosomal Drug Resistancementioning

confidence: 99%

A Novel Model of Cancer Drug Resistance: Oncosomal Release of Cytotoxic and Antibody-Based Drugs

Eguchi

Taha

Calderwood

et al. 2020

Biology

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“…EMT, almost by definition, enhances the motility and migration of tumor cells. It has been recently shown that cells release migrasomes during cell migration from cellular cilia, a tail of the cell [17,88]. The proteome of migrasomes was 27% common with exosomes, while the remaining 73% was specific to migrasomes [88].…”

Section: Exosomal Drug Resistancementioning

confidence: 99%

“…It has been recently shown that cells release migrasomes during cell migration from cellular cilia, a tail of the cell [17,88]. The proteome of migrasomes was 27% common with exosomes, while the remaining 73% was specific to migrasomes [88]. Therefore, EMT-driven migration of cancer cells may promote release of EVs including exosomes and migrasomes, which both may enhance the drug ejection, resistance phenotype of the cells.…”

Section: Exosomal Drug Resistancementioning

confidence: 99%

Exosome Release of Drugs: Coupling with Epithelial-Mesenchymal Transition

Eguchi¹,

Ono²,

Calderwood³

et al. 2019

Preprint

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Extracellular vesicles (EVs), such as exosomes or oncosomes are released with molecules unfavorable for survival from cells. In addition, accumulating evidence has shown that tumor cells often eject anti-cancer drugs such as chemotherapeutics and targeted drugs within EVs, a novel mechanism of drug resistance. The EV-releasing, drug resistance phenotype is often coupled with cellular dedifferentiation and transformation, cells undergoing epithelial-mesenchymal transition (EMT) and taking on a cancer stem cell phenotype. Recent studies have shown that the release of EVs is also involved in immunosuppression. The concept of the resistance-associated secretory phenotype (RASP) is reviewed herein.

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“…Recent works by Yu's group [26][27][28][29] discovered a unique class of microvesicles named as migrasomes can be secreted by cells during the process of cell migration. The studies showed that migrasomes have the following characteristics: (a) vesicles of 300-3,000 nm diameters with 1 monolar membrane, and (b) containing numerous smaller vesicles inside, and (c) expressing unique proteins such as NDST1 (bifunctionalheparan sulfate N-deacetylase/N-sulfotransferase 1), PIGK (phosphatidylinositol glycan anchor biosynthesis, class K), CPQ (carboxypeptidase Q), and EOGT (EGF domainspecific O-linked N acetylglucosaminetransferase).…”

Section: Introductionmentioning

confidence: 99%

Podocyte-Released Migrasomes in Urine Serve as an Indicator for Early Podocyte Injury

Liu

Rong

et al. 2020

Kidney Dis

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Background: Levels of urinary microvesicles, which are increased during various kidney injuries, have diagnostic potential for renal diseases. However, the significance of urinary microvesicles as a renal disease indicator is dampened by the difficulty to ascertain their cell source. Objectives: The aim of this study was to demonstrate that podocytes can release migrasomes, a unique class of microvesicle with size ranging between 400 and 2,000 nm, and the urine level of migrasomes may serve as novel non-invasive biomarker for early podocyte injury. Method: In this study, immunofluorescence labeling, electronic microscopy, nanosite, and sequential centrifugation were used to purify and analyze migrasomes. Results: Migrasomes released by podocytes differ from exosomes as they have different content and mechanism of release. Compared to podocytes, renal tubular cells secrete markedly less migrasomes. Moreover, secretion of migrasomes by human or murine podocytes was strongly augmented during podocyte injuries induced by LPS, puromycin amino nucleoside (PAN), or a high concentration of glucose (HG). LPS, PAN, or HG-induced podocyte migrasome release, however, was blocked by Rac-1 inhibitor. Strikingly, a higher level of podocyte migrasomes in urine was detected in mice with PAN-nephropathy than in control mice. In fact, increased urinary migrasome number was detected earlier than elevated proteinuria during PAN-nephropathy, suggesting that urinary migrasomes are a more sensitive podocyte injury indicator than proteinuria. Increased urinary migrasome number was also detected in diabetic nephropathy patients with proteinuria level <5.5 g/day. Conclusions: Our findings reveal that podocytes release the “injury-related” migrasomes during migration and provide urinary podocyte migrasome as a potential diagnostic marker for early podocyte injury.

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Identification of markers for migrasome detection

Cited by 81 publications

References 7 publications

A Novel Model of Cancer Drug Resistance: Oncosomal Release of Cytotoxic and Antibody-Based Drugs

A Novel Model of Cancer Drug Resistance: Oncosomal Release of Cytotoxic and Antibody-Based Drugs

Exosome Release of Drugs: Coupling with Epithelial-Mesenchymal Transition

Podocyte-Released Migrasomes in Urine Serve as an Indicator for Early Podocyte Injury

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