Publisher Correction: ITGB3-mediated uptake of small extracellular vesicles facilitates intercellular communication in breast cancer cells

Fuentes, Pedro Juan Barrios; Sesé, Marta; Guijarro, Pedro J.; Emperador, Marta; Sánchez‐Redondo, Sara; Peinado, Héctor; Hümmer, Stefan; Cajal, Santiago Ramón y

doi:10.1038/s41467-020-18674-4

Cited by 6 publications

(5 citation statements)

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“…Interestingly, these BAF-modulated integrins were also modulated after single inhibition of ARID1A or ARID1B, but to a lesser extent (Figure S7D), further highlighting the need for simultaneous inhibition of both proteins for full achievement of BAF inhibition effects. The functional consequences of this epigenetic event were supported by the protein reduction of the two most repressed integrins, namely, ITGB3 and ITGA9 (Figure 3G), both of which have been previously implicated in metastasis [36,37], as well as the clear repressive effect observed on transcriptional signatures related to the activation of integrin signalling (Figure S7E) and protein downregulation of key structural components of downstream pathways such as SRC or ILK, the last of which was transcriptionally and epigenetically repressed (Figure S7F-I).…”

Section: Baf Complex Disruption Promotes the Epigenetic Repression Of...mentioning

confidence: 69%

Structural disruption of BAF chromatin remodeller impairs neuroblastoma metastasis by reverting an invasiveness epigenomic program

Jiménez

Antonelli

Nadal-Ribelles

et al. 2022

Preprint

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BackgroundEpigenetic programming during development is essential for determining cell lineages, and alterations in this programming contribute to the initiation of embryonal tumour development. In neuroblastoma, neural crest progenitors block their course of natural differentiation into sympathoadrenergic cells, leading to the development of aggressive and metastatic paediatric cancer. Research of the epigenetic regulators responsible for oncogenic epigenomic networks is crucial for developing new epigenetic-based therapies against these tumours. Mammalian switch/sucrose non-fermenting (mSWI/SNF) ATP-dependent chromatin remodelling complexes act genome-wide translating epigenetic signals into open chromatin states. The present study aimed to understand the contribution of mSWI/SNF to the oncogenic epigenomes of neuroblastoma and its potential as a therapeutic target.MethodsFunctional characterisation of the mSWI/SNF complexes was performed in neuroblastoma cells using proteomic approaches, loss-of-function experiments, transcriptome and chromatin accessibility analyses, and in vitro and in vivo assays.ResultsNeuroblastoma cells contain three main mSWI/SNF subtypes, but only BRG1-associated factor (BAF) complex disruption through silencing of its key structural subunits, ARID1A and ARID1B, impairs cell proliferation by promoting cell cycle blockade. Genome-wide chromatin remodelling and transcriptomic analyses revealed that BAF disruption results in the epigenetic repression of an extensive invasiveness-related expression program involving integrins, cadherins, and key mesenchymal regulators, thereby reducing adhesion to the extracellular matrix and the subsequent invasion in vitro and drastically inhibiting the initiation and growth of neuroblastoma metastasis in vivo.ConclusionsWe report a novel ATPase-independent role for the BAF complex in maintaining an epigenomic program that allows neuroblastoma invasiveness and metastasis, urging for the development of new BAF pharmacological structural disruptors for therapeutic exploitation in metastatic neuroblastoma.

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Section: Baf Complex Disruption Promotes the Epigenetic Repression Of...mentioning

confidence: 69%

Structural disruption of BAF chromatin remodeller impairs neuroblastoma metastasis by reverting an invasiveness epigenomic program

Jiménez

Antonelli

Nadal-Ribelles

et al. 2022

Preprint

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“… 35 , 36 A number of related receptors and adhesion molecules on EV surface and recipient cells have been identified, including tetraspanins, integrins, proteoglycans, lectins, lipids, intercellular adhesion molecules and extracellular matrix components. 37 , 38 KIM-1 is originally identified as an early biomarker of renal proximal tubule injury. Recently, it has been confirmed that KIM-1 can function as a receptor recognizing PS, 39 oxidized low-density lipoprotein, 39 LMIR5/CD300b, 40 apoptosis inhibitor of macrophage, 41 and fatty acid.…”

Section: Discussionmentioning

confidence: 99%

KIM-1 augments hypoxia-induced tubulointerstitial inflammation through uptake of small extracellular vesicles by tubular epithelial cells

Chen¹,

Tang²,

Cao³

et al. 2023

Molecular Therapy

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“…Recent studies revealed that EVs may be internalized by host cells by clathrin-independent endocytosis, especially caveolae-dependent endocytosis. , However, different types of cells may differ in the specific mechanism of EV uptake. On the other hand, proteins localized on the surface of EVs, such as integrins and proteoglycans, play a vital role in the internalization of EVs . Research indicated that glycans in the surface of EVs could bind to the cellular chemokine receptor CCR8 via a bridging chemokine .…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, proteins localized on the surface of EVs, such as integrins and proteoglycans, play a vital role in the internalization of EVs. 43 Research indicated that glycans in the surface of EVs could bind to the cellular chemokine receptor CCR8 via a bridging chemokine. 44 The functional status of recipient cells also could influence the uptake of EVs.…”

Section: Conclusion Msc-derivedmentioning

confidence: 99%

Engineering Extracellular Vesicles Restore the Impaired Cellular Uptake and Attenuate Intervertebral Disc Degeneration

Liao

Liu

et al. 2021

ACS Nano

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Extracellular vesicles (EVs) are potential alternatives for mesenchymal stem cells (MSCs) in the treatment of musculoskeletal degenerative diseases, including intervertebral disc degeneration (IDD). Usually, EVs are internalized and then deliver bioactive molecules that impart phenotypic changes in recipient cells. For effective utilization of EVs in the IDD therapy, understanding the mechanism of EV uptake is of vital importance. In this study, we found that EVs delivered antioxidant proteins to protect against pyroptosis of nucleus pulposus cells (NPCs). In particular, the therapeutic effect of EVs decreased in TNF-α-treated NPCs due to the impaired caveolae-mediated endocytosis pathway. Transcriptome sequencing and functional verification revealed that caveolae associated protein 2 (Cavin-2) played an important role in the uptake process of EVs. We then constructed the Cavin-2-modified engineering EVs via the gene-editing of parental MSCs. These kinds of modified EVs presented an improved uptake rate in TNF-α-treated NPCs, which effectively ameliorated the cell death of NPCs in a three-dimensional hydrogel culture model and retarded the progression of IDD in the ex vivo organ culture model. Collectively, these findings illustrate the mechanism of EV uptake in NPCs and explore the application of engineering EVs in the treatment of IDD.

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Publisher Correction: ITGB3-mediated uptake of small extracellular vesicles facilitates intercellular communication in breast cancer cells

Abstract: An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Cited by 6 publications

References 0 publications

Structural disruption of BAF chromatin remodeller impairs neuroblastoma metastasis by reverting an invasiveness epigenomic program

Structural disruption of BAF chromatin remodeller impairs neuroblastoma metastasis by reverting an invasiveness epigenomic program

KIM-1 augments hypoxia-induced tubulointerstitial inflammation through uptake of small extracellular vesicles by tubular epithelial cells

Engineering Extracellular Vesicles Restore the Impaired Cellular Uptake and Attenuate Intervertebral Disc Degeneration

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