Exosomes in cancer: Use them or target them?

Bastos, Nuno; Ruivo, Carolina F.; Silva, Soraia da; Melo, Sónia A.

doi:10.1016/j.semcdb.2017.08.009

Cited by 116 publications

(76 citation statements)

References 97 publications

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“…Copyright (2017) American Chemical Society inhibition of the exosome production, secretion, cell-tocell communication as well as removal of exosomalspecific loads [179,180]. Also given their stability in systemic circulation and tumor-based specificity, exosomes are studied for their abilities to deliver anti-cancer agents [181].…”

Section: Exosomesmentioning

confidence: 99%

Tumor microenvironment complexity and therapeutic implications at a glance

et al. 2020

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The dynamic interactions of cancer cells with their microenvironment consisting of stromal cells (cellular part) and extracellular matrix (ECM) components (non-cellular) is essential to stimulate the heterogeneity of cancer cell, clonal evolution and to increase the multidrug resistance ending in cancer cell progression and metastasis. The reciprocal cell-cell/ECM interaction and tumor cell hijacking of non-malignant cells force stromal cells to lose their function and acquire new phenotypes that promote development and invasion of tumor cells. Understanding the underlying cellular and molecular mechanisms governing these interactions can be used as a novel strategy to indirectly disrupt cancer cell interplay and contribute to the development of efficient and safe therapeutic strategies to fight cancer. Furthermore, the tumor-derived circulating materials can also be used as cancer diagnostic tools to precisely predict and monitor the outcome of therapy. This review evaluates such potentials in various advanced cancer models, with a focus on 3D systems as well as lab-on-chip devices.

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Section: Exosomesmentioning

confidence: 99%

Tumor microenvironment complexity and therapeutic implications at a glance

et al. 2020

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“…Interestingly, miRNAs are present both in the cytosol of the irradiated cells and within exosomes released by those cells, where they are encapsulated to deliver information to neighbouring cells. These tumour‐derived micro‐vesicles are now recognized as crucial mechanisms for cell–cell communication, delivering genetic information to recipient cells in the tumour environment (Al‐Mayah et al , ; King, Michael, & Gleadle, ; Rupaimoole et al , ; Tsang et al , ; Bastos et al , ), and thus playing an important role in cancer metastasis and prognosis (Fujita et al , ). Once tumour‐derived micro‐vesicles have been released, they are harvested by recipient cells that have survived therapy, inducing alterations that lead to tumour repopulation via the regulation of crucial signalling pathways (Skog et al , ; Katsuda, Kosaka, & Ochiya, ).…”

Section: Oncometabolites and Tumour Repopulationmentioning

confidence: 99%

Oncometabolites in cancer aggressiveness and tumour repopulation

et al. 2019

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Tumour repopulation is recognized as a crucial event in tumour relapse where therapy-sensitive dying cancer cells influence the tumour microenvironment to sustain therapy-resistant cancer cell growth. Recent studies highlight the role of the oncometabolites succinate, fumarate, and 2-hydroxyglutarate in the aggressiveness of cancer cells and in the worsening of the patient's clinical outcome. These oncometabolites can be produced and secreted by cancer and/or surrounding cells, modifying the tumour microenvironment and sustaining an invasive neoplastic phenotype. In this review, we report recent findings concerning the role in cancer development of succinate, fumarate, and 2-hydroxyglutarate and the regulation of their related enzymes succinate dehydrogenase, fumarate hydratase, and isocitrate dehydrogenase. We propose that oncometabolites are crucially involved in tumour repopulation. The study of the mechanisms underlying the relationship between oncometabolites and tumour repopulation is fundamental for identifying efficient anti-cancer therapeutic strategies and novel serum biomarkers in order to overcome cancer relapse.

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“…EVs uptake was improved by extracellular proteins as albumin, but was inhibited by cigarette smoke extract, via oxidative dysfunction of actin polymerization 31 . Taken together, these data indicate that EVs internalization is not a passive process 32 and different kind of cells can internalize EVs with a specific mechanism. Actually, EVs subcellular fate within recipient cells and their mechanisms of cargo release remain unclear.…”

mentioning

confidence: 62%