Extracellular Vesicles and Epigenetic Modifications Are Hallmarks of Melanoma Progression

Abstract

Cutaneous melanoma shows a high metastatic potential based on its ability to overcome the immune system’s control. The mechanisms activated for these functions vary extremely and are also represented by the production of a number of extracellular vesicles including exosomes. Other vesicles showing a potential role in the melanoma progression include oncosomes and melanosomes and the majority of them mediate tumor processes including angiogenesis, immune regulation, and modifications of the micro-environment. Moreover, a number of epigenetic modifications have been described in melanoma and abundant production of altered microRNAs (mi-RNAs), non-coding RNAs, histones, and abnormal DNA methylation have been associated with different phases of melanoma progression. In addition, exosomes, miRNAs, and other molecular factors have been used as potential biomarkers reflecting disease evolution while others have been suggested to be potential druggable molecules for therapeutic application.

Extracellular Vesicles Function as Bioactive Molecular Transmitters in the Mammalian Oviduct: An Inspiration for Optimizing in Vitro Culture Systems and Improving Delivery of Exogenous Nucleic Acids during Preimplantation Embryonic Development

“…The L-EVs, larger vesicles than 200 nm, include microvesicles/ectosomes, apoptotic bodies and large oncosomes, while S-EVs include exosomes and exomeres. Microvesicles (0.2-0.5 µm) are large extracellular vesicles originated from the plasma membrane by direct shedding in response to cellular activation or stress, apparently in a manner similar to that of retroviruses [20][21][22][23][24]. Baig et al [25] also found that microvesicles originate at special lipid raft domains of the plasma membrane.…”

“…Baig et al [25] also found that microvesicles originate at special lipid raft domains of the plasma membrane. When cells undergo apoptosis, they dissociate into membrane-bound apoptotic bodies (0.8-5 µm), which might contain genomic DNA [20,26]. In addition, in cancer cells, the larger EVs (1-10 µm), termed large oncosomes, can bleb off the cell membrane [20,27].…”

“…When cells undergo apoptosis, they dissociate into membrane-bound apoptotic bodies (0.8-5 µm), which might contain genomic DNA [20,26]. In addition, in cancer cells, the larger EVs (1-10 µm), termed large oncosomes, can bleb off the cell membrane [20,27]. Exosomes (50-100 nm), a subclass of (S)-EVs, are produced via lyso-endosomal pathways.…”

Application of “omics” sciences to the prediction of bone metastases from breast cancer: State of the art

“…Even if not encoding protein products, noncoding RNA (ncRNAs) are critical regulators of cellular processes. In particular, miRNAs are small (approximately 22 base pairs) ncRNAs that act as epigenetic modulators by targeting the turnover of specific mRNAs, through which they regulate a huge number of processes, including signal transduction, cell cycle, cell proliferation and metabolism, all of them playing key roles in cancer [68] , [69] . miRNAs have been investigated for their capability to participate in the bone homing process and act as potential biomarkers of BC skeletal colonization ( Table 2 ).…”

Liquid Biopsy as a Tool Exploring in Real-Time Both Genomic Perturbation and Resistance to EGFR Antagonists in Colorectal Cancer

“…Those bearing a nano-sized diameter (30-100 nm) are currently referred to as small-EVs or Exo (63,64). They are involved in intercellular communication by delivering cargos of active molecules including proteins, messenger RNAs, non-coding RNAs, and DNA fragments from one to another cell (65). Many studies in CRC revealed that Exo are involved in tumor progression and metastasis, as well as in tumor resistance against either cytotoxic or targeting agents (66,67).…”