Exosomal Lipids in Cancer Progression and Metastasis

Cancer Medicine, Journal Year: 2025, Volume and Issue: 14(6)

Published: March 1, 2025

Metastasis is the primary cause of cancer mortality. It responsible for 90% all cancer-related deaths. Intercellular communication a crucial feature underlying metastasis and progression. Cancerous tumors secrete membrane-derived small extracellular vesicles (30-150 nm) into their milieu. These tiny organelles, known as exosomes, facilitate intercellular by transferring bioactive molecules. exosomes harbor different cargos, such proteins, nucleic acids, lipids, that mediate multifaceted functions in various oncogenic processes. Of note, amount lipids multifold higher than other cargos. Most studies have investigated role exosomes' protein acid content processes, while lipid cargo pathophysiology remains largely obscure. We conducted an extensive literature review on progression, specifically addressing topic exosomal involvement This aims to shed light contents metastasis. In this context, signaling pathways, immunomodulation, energy production cell survival provides insights overcoming progression

Language: Английский

Epigenetic Inactivation of RIPK3-Dependent Necroptosis Augments Cisplatin Chemoresistance in Human Osteosarcoma

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(8), P. 3863 - 3863

Published: April 18, 2025

Osteosarcoma (OS) is the most common primary bone malignancy in children and adolescents. Unfortunately, drug resistance limits efficacy of chemotherapeutic treatment compromises therapeutic outcomes a substantial proportion cases. Aberrant CpG island methylation-associated transcriptional silencing contributes to chemoresistance pediatric solid tumors. Here, using whole-genome DNA methylation screening on 16 human OS specimens, we identify receptor interacting protein kinase-3 (RIPK3), molecular regulator necroptosis programmed cell death pathway, as gene target aberrant demonstrate its role chemoresistance. We validated these findings via enforced expression DsiRNA silencing, evaluated RIPK3 cisplatin chemosensitivity activation through MLKL phosphorylation. found that results samples lines. Enforced significantly enhanced cytotoxicity cells knockdown reversed cisplatin-sensitive phenotype. In with expression, increased phosphorylation both target, MLKL, indicative induction necroptosis. an important mediator potential pharmacologic improve chemotherapy drug-resistant

Language: Английский