Extracellular vesicles as regulators of tumor fate: crosstalk among cancer stem cells, tumor cells and mesenchymal stem cells

Lindoso, Rafael Soares; Collino, Federica; Vieyra, Adalberto

doi:10.21037/sci.2017.08.08

Cited by 46 publications

(47 citation statements)

References 127 publications

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“…Indeed, in a spontaneous murine model of melanoma, MDSCs induce EMT via TGF- β , EGF, and HGF signaling [ 75 ]. Similarly, platelet-derived TGF- β secreted by MDSCs activates TGF- β /Smad and NF- κ B pathways in lung cancer cells, resulting in EMT and enhanced metastasis in vivo , in lung cancer models [ 76 , 77 ].…”

Section: Tumor Microenvironment and Cancer Cell Phenotypementioning

confidence: 99%

Dynamism, Sensitivity, and Consequences of Mesenchymal and Stem-Like Phenotype of Cancer Cells

Gener

Seras‐Franzoso

Callejo

et al. 2018

Stem Cells International

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There are remarkable similarities in the description of cancer stem cells (CSCs) and cancer cells with mesenchymal phenotype. Both cell types are highly tumorigenic, resistant against common anticancer treatment, and thought to cause metastatic growth. Moreover, cancer cells are able to switch between CSC and non-CSC phenotypes and vice versa, to ensure the necessary balance within the tumor. Likewise, cancer cells can switch between epithelial and mesenchymal phenotypes via well-described transition (EMT/MET) that is thought to be crucial for tumor propagation. In this review, we discuss whether, and to which extend, the CSCs and mesenchymal cancer cells are overlapping phenomena in terms of mechanisms, origin, and implication for cancer treatment. As well, we describe the dynamism of both phenotypes and involvement of the tumor microenvironment in CSC reversion and in EMT.

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Section: Tumor Microenvironment and Cancer Cell Phenotypementioning

confidence: 99%

Dynamism, Sensitivity, and Consequences of Mesenchymal and Stem-Like Phenotype of Cancer Cells

Gener

Seras‐Franzoso

Callejo

et al. 2018

Stem Cells International

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“…Growing evidence suggests that intercellular communication of injured ECs with the EVs released in vitro by the cultured bone marrow-derived MSCs (EV MSC ) hold significant therapeutic promise for ARDS [ 6 ]. EVs are released from a variety of cells as byproducts of cell growth, apoptosis and in response to physiologic and pathophysiologic stimuli [ 7 ]. These EVs, also known as microparticles, microvesicles, microsomes, lipid vesicles and exosomes encapsulate small portions of the subjacent cytosol, creating a heterogeneous population of phospholipid-walled vesicles [ 7 , 8 ].…”

Section: Introductionmentioning

confidence: 99%

“…EVs are released from a variety of cells as byproducts of cell growth, apoptosis and in response to physiologic and pathophysiologic stimuli [ 7 ]. These EVs, also known as microparticles, microvesicles, microsomes, lipid vesicles and exosomes encapsulate small portions of the subjacent cytosol, creating a heterogeneous population of phospholipid-walled vesicles [ 7 , 8 ]. The EVs circulate in the blood for an unknown length of time, interact with ECs and depending on their cellular origin/cargo may have different effects on EC function [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

Alk5/Runx1 signaling mediated by extracellular vesicles promotes vascular repair in acute respiratory distress syndrome

Shah

Qin

Vashi

et al. 2018

Clinical & Translational Med

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Background Pulmonary endothelial cells’ (ECs) injury and apoptotic death are necessary and sufficient for the pathogenesis of the acute respiratory distress syndrome (ARDS), regardless of epithelial damage. Interaction of dysfunctional ECs with circulatory extracellular vesicles (EVs) holds therapeutic promise in ARDS. However, the presence in the blood of long-term ARDS survivors of EVs with a distinct phenotype compared to the EVs of non-surviving patients is not reported. With a multidisciplinary translational approach, we studied EVs from the blood of 33 patients with moderate-to-severe ARDS. Results The EVs were isolated from the blood of ARDS and control subjects. Immunoblotting and magnetic beads immunoisolation complemented by standardized flow cytometry and nanoparticles tracking analyses identified in the ARDS patients a subset of EVs with mesenchymal stem cell (MSC) origin (CD73 + CD105 + Cd34 − CD45 − ). These EVs have 4.7-fold greater counts compared to controls and comprise the transforming growth factor-beta receptor I (TβRI)/Alk5 and the Runx1 transcription factor. Time course analyses showed that the expression pattern of two Runx1 isoforms is critical for ARDS outcome: the p52 isoform shows a continuous expression, while the p66 is short-lived. A high ratio Runx1p66 / p52 provided a survival advantage, regardless of age, sex, disease severity or length of stay in the intensive care unit. Moreover, the Runx1p66 isoform is transiently expressed by cultured human bone marrow-derived MSCs, it is released in the EVs recoverable from the conditioned media and stimulates the proliferation of lipopolysaccharide (LPS)-treated ECs. The findings are consistent with a causal effect of Runx1p66 expression on EC proliferation. Furthermore, morphological and functional assays showed that the EVs bearing the Runx1p66 enhanced junctional integrity of LPS-injured ECs and decreased lung histological severity in the LPS-treated mice. Conclusions The expression pattern of Runx1 isoforms might be a reliable circulatory biomarker of ARDS activity and a novel determinant of the molecular mechanism for lung vascular/tissue repair and recovery after severe injury. Electronic supplementary material The online version of this article (10.1186/s40169-018-0197-2) contains supplementary material, which is available to authorized users.

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“…Indeed, EVs are able to spread oncogenic messages through RNAs and proteins that regulate important processes inside the cells, such as proliferation, differentiation, survival, and migratory ability in different tumor types, including HCC [31][32][33]. Finally, EVs also participate in inflammatory processes, angiogenesis, extracellular matrix remodeling, the formation of the metastatic niche, and inhibition of the antitumor immune response [11].…”

Section: Overview Of Extracellular Vesiclesmentioning

confidence: 99%

Extracellular Vesicles, A Possible Theranostic Platform Strategy for Hepatocellular Carcinoma—An Overview

D’Agnano

Berardi

2020

Cancers

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Hepatocellular carcinoma (HCC) is the sixth most common cancer and the third highest cause of mortality from cancer, largely because of delays in diagnosis. There is currently no effective therapy for advanced stage HCC, although sorafenib, the standard treatment for HCC, systemic therapy (including tyrosine kinase inhibitors and anti-angiogenesis agents), and more recently, immunotherapy, have demonstrated some survival benefit. The measurement and modification of extracellular vesicle (EVs) cargoes—composed of nucleic acids, including miRNAs, proteins, and lipids—holds great promise for future HCC diagnosis, prognosis, and treatment. This review will provide an overview of the most recent findings regarding EVs in HCC, and the possible future use of EVs as “liquid biopsy”-based biomarkers for early diagnosis and as a vehicle for targeted drug-delivery.

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Extracellular vesicles as regulators of tumor fate: crosstalk among cancer stem cells, tumor cells and mesenchymal stem cells

Cited by 46 publications

References 127 publications

Dynamism, Sensitivity, and Consequences of Mesenchymal and Stem-Like Phenotype of Cancer Cells

Dynamism, Sensitivity, and Consequences of Mesenchymal and Stem-Like Phenotype of Cancer Cells

Alk5/Runx1 signaling mediated by extracellular vesicles promotes vascular repair in acute respiratory distress syndrome

Extracellular Vesicles, A Possible Theranostic Platform Strategy for Hepatocellular Carcinoma—An Overview

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