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Cancer is a major health burden worldwide. Despite the advances in our understanding of its pathogenesis and continued improvement in cancer management and outcomes, there remains a strong clinical demand for more accurate and reliable biomarkers of metastatic progression and novel therapeutic targets to abrogate angiogenesis and tumour progression. Aquaporin 1 (AQP1) is a small hydrophobic integral transmembrane protein with a predominant role in trans-cellular water transport. Recently, over-expression of AQP1 has been associated with many types of cancer as a distinctive clinical prognostic factor. This has prompted researchers to evaluate the link between AQP1 and cancer biological functions. Available literature implicates the role of AQP1 in tumour cell migration, invasion and angiogenesis. This article reviews the current understanding of AQP1-facilitated tumour development and progression with a focus on regulatory mechanisms and downstream signalling pathways.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5343835 | PMC |
http://dx.doi.org/10.3390/ijms18020299 | DOI Listing |
Adv Sci (Weinh)
September 2025
Department of Physics, State Key Laboratory of Surface Physics, and Key Laboratory for Computational Physical Science (Ministry of Education), Fudan University, 2005 Songhu Road, Yangpu District, Shanghai, 200433, China.
Emerging evidence indicates that liquid-liquid phase separation of α-synuclein occurs during the nucleation step of its aggregation, a pivotal step in the onset of Parkinson's disease. Elucidating the molecular determinants governing this process is essential for understanding the pathological mechanisms of diseases and developing therapeutic strategies that target early-stage aggregation. While previous studies have identified residues critical for α-synuclein amyloid formation, the key residues and molecular drivers of its phase separation remain largely unexplored.
View Article and Find Full Text PDFDevelopment
September 2025
MRC Laboratory of Molecular Biology, Cambridge CB2 0QH, UK.
In an era of expanding reproductive possibilities, the human embryo has come to represent both immense potential and profound constraint. Advances in medically assisted reproduction (MAR) have led to the cryopreservation of hundreds of thousands of embryos each year, yet many remain unused and are ultimately discarded. Meanwhile, studies aimed at understanding infertility, early human development and preventing miscarriage continue to face significant barriers, with only a small fraction of embryos ever donated to research.
View Article and Find Full Text PDFJ Pathol Transl Med
September 2025
Department of Otorhinolaryngology Head and Neck Surgery, Affiliated Hospital of Guizhou Medical University, Guiyang, China.
Background: C-C motif chemokine ligand 3 (CCL3) is a crucial chemokine that plays a fundamental role in the immune microenvironment and is closely linked to the development of various cancers. Despite its importance, there is limited research regarding the expression and function of CCL3 in nasopharyngeal carcinoma (NPC). Therefore, this study seeks to examine the expression of CCL3 and assess its clinical significance in NPC using bioinformatics analysis and experiments.
View Article and Find Full Text PDFCell Physiol Biochem
September 2025
Department of Histology and Embryology and Vascular Biology Student Research Club, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Torun, 85-092 Bydgoszcz, Poland, E-Mail:
Migrasomes are newly discovered, migration-dependent organelles that mediate the release of cellular contents into the extracellular environment through a process known as migracytosis. Since their identification in 2014, growing evidence has highlighted their critical roles in intercellular communication, organ development, mitochondrial quality control, and disease pathogenesis. Migrasome biogenesis is a complex, multi-step process tightly regulated by lipid composition, tetraspanin-enriched microdomains, and molecular pathways involving sphingomyelin synthase 2, Rab35, and integrins.
View Article and Find Full Text PDFMacrophage Migration Inhibitory Factor (MIF) is a pleiotropic cytokine that acts as a central regulator of inflammation and immune responses across diverse organ systems. Functioning upstream in immune activation cascades, MIF influences macrophage polarization, T and B cell differentiation, and cytokine expression through CD74, CXCR2/4/7, and downstream signaling via NF-κB, ERK1/2, and PI3K/AKT pathways. This review provides a comprehensive analysis of MIF's mechanistic functions under both physiological and pathological conditions, highlighting its dual role as a protective mediator during acute stress and as a pro-inflammatory amplifier in chronic disease.
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