Breast cancer (BC) constitutes the most prevalent malignancy globally, with an incidence of approximately 80%-85% for invasive ductal carcinoma (IDC) and 10%-15% for invasive lobular carcinoma (ILC), and a persistently high mortality and morbidity rate. Although IDC and ILC originate from distinct cellular lineages (ductal and lobular epithelial cells, respectively), they frequently develop in the context of hormonal dysregulation and chronic proliferative stimuli. Recent evidence accumulated over the past decade has demonstrated a role for cytokines belonging to the interleukin-6 (IL-6) family in the pathogenesis and progression of BC. These cytokines exert their effects via the activator of transcription (JAK/STAT) pathways, activating downstream Janus kinase/signal transducer, and gp130 receptor subunit activation. As a member of the IL-6 family, Oncostatin M (OSM.) is critically involved in the processes of autoimmune disorders, inflammation, and oncogenesis, particularly in BC. It has been demonstrated that the overexpression of OSM and OSM receptor (OSMR) plays a pivotal role in cancer cell remodeling and promotes cell proliferation, angiogenesis, survival, invasion, and other hallmark features of BC. However, owing to the involvement of multiple signaling pathways, OSM can exert context-dependent and even contradictory effects in certain cancer types. This review aims to examine the emerging roles of OSM in BC, elucidate its multifunctional role in tumor regulation and progression, and ultimately explore therapeutic strategies developed to modulate this cytokine in the context of BC.
Muslem Nuseir, Farrukh Ismatov, A. Abdulqader et al.· IUBMB Life - A Journal of th...· 0 citations
Neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and Huntington's disease are among the progressive disorders of the nervous system that are characterized by the gradual destruction of neurons, the accumulation of misfolded proteins, and the limited effective therapeutic options. In recent years, numerous lines of evidence have emphasized the important role of extracellular vesicles (EVs) in the formation and progression of these diseases. These vesicles are membrane-bound nanoscale structures that are secreted by almost all cell types and play a role in cell-cell communication through the transfer of molecules such as proteins, lipids, and nucleic acids. In neurodegenerative disorders, EVs can facilitate the transport and dissemination of disease-related proteins, including amyloid-β, tau, α-synuclein, mutant huntingtin, SOD1, and TDP-43, thus contributing to the spread of pathological processes in different parts of the nervous system. On the other hand, the ability of these vesicles to cross the blood-brain barrier and reflect molecular changes occurring in the central nervous system makes them valuable candidates for the development of minimally invasive biomarkers. This review reviews the biogenesis, classification, isolation methods, and molecular content of EVs, and analyzes their role in the pathogenesis, diagnosis, and treatment of the most important neurodegenerative diseases. Also, the importance of EV-associated proteins, RNAs, and lipids as emerging diagnostic biomarkers, as well as the therapeutic potential of natural and engineered vesicles as drug delivery systems and regulators of neuroinflammation and neurodegenerative processes, is discussed.
S. Mohammad, A. Vasudevan, G. Oriquat et al.· Behavioural Brain Research· 0 citations
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