Extracellular Vesicles and Resistance to Anticancer Drugs: A Tumor Skeleton Key for Unhinging Chemotherapies

Pompili, Simona; Vetuschi, Antonella; Sferra, Roberta; Cappariello, Alfredo

doi:10.3389/fonc.2022.933675

Cited by 10 publications

(3 citation statements)

References 179 publications

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“…Nevertheless, an increase in average number EVs in drug treated vin tolerant lines was observed, which can be further supported with literature, where it has also indicated that EVs can act as transporters for efflux of drugs. 23 Thus it can be concluded that number of EVs are enhanced in drug tolerant lines which together with EC50 data suggest EV mediated drug tolerance in medulloblastoma cell lines.…”

Section: Drug Resistance In Medulloblastomasmentioning

confidence: 85%

Tackling Anticancer Drug Resistance and Endosomal Escape in Aggressive Brain Tumors Using Bioelectronics

Jain,

Wade,

Stolnik

et al. 2024

Preprint

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Chemotherapy resistance and endosomal entrapment, controlled by intracellular trafficking processes, are major factor in treatment failure. Here, we test the hypothesis that external electrical stimulus can be used to modulate intracellular trafficking of chemotherapeutic drugs in most common malignant brain tumors in childhood (medulloblastoma) and gold nanoparticles (GNPs) in adulthood (glioblastoma). We demonstrate that application of alternating current (AC) with frequencies ranging from KHz-MHz and low strength (1 V/cm) lead to killing of cisplatin and vincristine resistant (mediated by extracellular vesicles) medulloblastoma cell lines. On the other hand, in primary glioblastoma cells high frequency AC (MHz) regulated the endosomal escape of GNPs. No significant effect on the viability of the control medulloblastoma cells (resistant cells cultured in drug free media and non-resistant cells) and glioblastoma cells after AC treatment confirmed targeting of intracellular trafficking process. This work supports future application of AC in drug delivery and brain cancer therapy.

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Section: Drug Resistance In Medulloblastomasmentioning

confidence: 85%

Tackling Anticancer Drug Resistance and Endosomal Escape in Aggressive Brain Tumors Using Bioelectronics

Jain,

Wade,

Stolnik

et al. 2024

Preprint

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“…It exerts its anti-fibrotic effects by antagonizing TGFβ-induced EMT and promoting tissue repair and regeneration. GED-0507-34 Levo is an orally active synthetic compound and a selective agonist of PPARγ that has been shown to inhibit EMT, reduce inflammation, and ameliorate fibrosis in a DSS model (Di Gregorio et al, 2017;Pompili et al, 2023). In fact, GED-0507-34 is in a Phase 2 clinical trial in subjects with active, mild-tomoderate UC (ClinicalTrials.gov Identifier: NCT02808390).…”

Section: Proteinmentioning

confidence: 99%

Role of the epithelial barrier in intestinal fibrosis associated with inflammatory bowel disease: relevance of the epithelial-to mesenchymal transition

Macias-Ceja,

Mendoza-Ballesteros,

Ortega-Albiach

et al. 2023

Front. Cell Dev. Biol.

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In inflammatory bowel disease (IBD), chronic inflammation in the gastrointestinal tract can lead to tissue damage and remodelling, which can ultimately result in fibrosis. Prolonged injury and inflammation can trigger the activation of fibroblasts and extracellular matrix (ECM) components. As fibrosis progresses, the tissue becomes increasingly stiff and less functional, which can lead to complications such as intestinal strictures, obstructive symptoms, and eventually, organ dysfunction. Epithelial cells play a key role in fibrosis, as they secrete cytokines and growth factors that promote fibroblast activation and ECM deposition. Additionally, epithelial cells can undergo a process called epithelial-mesenchymal transition, in which they acquire a more mesenchymal-like phenotype and contribute directly to fibroblast activation and ECM deposition. Overall, the interactions between epithelial cells, immune cells, and fibroblasts play a critical role in the development and progression of fibrosis in IBD. Understanding these complex interactions may provide new targets for therapeutic interventions to prevent or treat fibrosis in IBD. In this review, we have collected and discussed the recent literature highlighting the contribution of epithelial cells to the pathogenesis of the fibrotic complications of IBD, including evidence of EMT, the epigenetic control of the EMT, the potential influence of the intestinal microbiome in EMT, and the possible therapeutic strategies to target EMT. Finally we discuss the pro-fibrotic interactions epithelial-immune cells and epithelial-fibroblasts cells.

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“…Furthermore, ADM-resistant cell-derived sEVs endow sensitive cells with a drug-resistant phenotype [ 76 ]. Evidence shows that drug-resistant tumor cells gain chemoresistance by encasing chemotherapeutic drugs into sEVs and excreting them [ 169 , 170 ]. sEVs contain a large amount of genetic material and are exchanged among cells in TME.…”

Section: Tumor-derived Sevs Play Vital Roles In the Bc Microenvironmentmentioning

confidence: 99%

Tumor-Derived Small Extracellular Vesicles Involved in Breast Cancer Progression and Drug Resistance

Feng

Guo

Tanaka

et al. 2022

IJMS

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Breast cancer is one of the most serious and terrifying threats to the health of women. Recent studies have demonstrated that interaction among cancer cells themselves and those with other cells, including immune cells, in a tumor microenvironment potentially and intrinsically regulate and determine cancer progression and metastasis. Small extracellular vesicles (sEVs), a type of lipid-bilayer particles derived from cells, with a size of less than 200 nm, are recognized as one form of important mediators in cell-to-cell communication. sEVs can transport a variety of bioactive substances, including proteins, RNAs, and lipids. Accumulating evidence has revealed that sEVs play a crucial role in cancer development and progression, with a significant impact on proliferation, invasion, and metastasis. In addition, sEVs systematically coordinate physiological and pathological processes, such as coagulation, vascular leakage, and stromal cell reprogramming, to bring about premetastatic niche formation and to determine metastatic organ tropism. There are a variety of oncogenic factors in tumor-derived sEVs that mediate cellular communication between local stromal cells and distal microenvironment, both of which are important in cancer progression and metastasis. Tumor-derived sEVs contain substances that are similar to parental tumor cells, and as such, sEVs could be biomarkers in cancer progression and potential therapeutic targets, particularly for predicting and preventing future metastatic development. Here, we review the mechanisms underlying the regulation by tumor-derived sEVs on cancer development and progression, including proliferation, metastasis, drug resistance, and immunosuppression, which coordinately shape the pro-metastatic microenvironment. In addition, we describe the application of sEVs to the development of cancer biomarkers and potential therapeutic modalities and discuss how they can be engineered and translated into clinical practice.

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Extracellular Vesicles and Resistance to Anticancer Drugs: A Tumor Skeleton Key for Unhinging Chemotherapies

Cited by 10 publications

References 179 publications

Tackling Anticancer Drug Resistance and Endosomal Escape in Aggressive Brain Tumors Using Bioelectronics

Tackling Anticancer Drug Resistance and Endosomal Escape in Aggressive Brain Tumors Using Bioelectronics

Role of the epithelial barrier in intestinal fibrosis associated with inflammatory bowel disease: relevance of the epithelial-to mesenchymal transition

Tumor-Derived Small Extracellular Vesicles Involved in Breast Cancer Progression and Drug Resistance

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