Department of Surgery, University of Melbourne, Cell Signaling Laboratory, Level 5, Clinical Sciences Building, Royal Melbourne Hospital, Parkville, Victoria 3050, Australia.
Published: July 2008
AI Article Synopsis
Article Abstract
Invasion of tissues by malignant tumours is facilitated by tumour cell migration and degradation of extracellular matrix (ECM) barriers. Several invasive neoplasms, including head and neck squamous cell carcinoma, breast carcinoma, melanoma and glioma, contain tumour cells that can form actin-rich protrusions with ECM proteolytic activity called invadopodia. These dynamic organelle-like structures adhere to, and digest, collagens, laminins and fibronectin. Invadopodia are dependent on multiple transmembrane, cytoplasmic and secreted proteins engaged in cell adhesion, signal transduction, actin assembly, membrane regulation and ECM proteolysis. Strategies aimed at disrupting invadopodia could form the basis of novel anti-invasive therapies for treating patients. Here we review the molecular basis of invadopodia formation with particular emphasis on the intracellular signaling networks that are essential for invadopodia activity and examine the potential role of these structures in glioma invasion.
NADPH oxidases (NOX) are membrane-bound proteins involved in the localized generation of reactive oxygen species (ROS) at the cellular surface. In cancer, these highly reactive molecules primarily originate in mitochondria and via NOX, playing a crucial role in regulating fundamental cellular processes such as cell survival, angiogenesis, migration, invasion, and metastasis. The NOX protein family comprises seven members (NOX1-5 and DUOX1-2), each sharing a catalytic domain and an intracellular dehydrogenase site.
Autoimmune glomerulonephritis is a homogeneous area of renal pathology with clinical relevance in terms of its numerical impact and difficulties in its treatment. Systemic lupus erythematosus/lupus nephritis and membranous nephropathy are the two most frequent autoimmune conditions with clinical relevance. They are characterized by glomerular deposition of circulating autoantibodies that recognize glomerular antigens.
Objective: The study aimed to investigate the expression of hypoxia markers associated with invadopodia in glandular odontogenic cysts and to explore an association between this expression with the aggressive biological behaviour of this odontogenic cyst.
Design: Immunohistochemistry was employed to assess the expression of hypoxia-inducible factor 1 alpha (HIF-1α), notch homologous protein of the neurogenic locus 1 (NOTCH-1), disintegrin and metalloproteinase-12 (ADAM-12), and heparin-binding epidermal growth factor (HB-EGF) in 17 samples of glandular odontogenic cysts, 10 samples of calcifying odontogenic cysts, and 10 samples of dental follicles.
Results: The glandular odontogenic cyst samples exhibited increased expression of HIF-1α, NOTCH-1, ADAM-12 and HBEGF proteins compared with calcifying odontogenic cyst and dental follicle samples.
Rufy4, a protein belonging to the RUN and FYVE domain-containing protein family, participates in various cellular processes such as autophagy and intracellular trafficking. However, its role in osteoclast-mediated bone resorption remains uncertain. In this study, we investigated the expression and role of the gene in osteoclasts using small interfering RNA (siRNA) transfection and gene overexpression systems.
Preclinical Models and New Therapeutic Agents Unit, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Regina Elena National Cancer Institute, Rome, Italy.
The high-grade serous ovarian cancer (HG-SOC) is a notoriously challenging disease, characterized by a rapid peritoneal dissemination. HG-SOC cells leverage actin-rich membrane protrusions, known as invadopodia, to degrade the surrounding extracellular matrix (ECM) and invade, initiating the metastatic cascade. In HG-SOC, the endothelin-1 (ET-1)/endothelin A receptor (ETAR)-driven signaling coordinates invadopodia activity, however how this axis integrates pro-oncogenic signaling routes, as YAP-driven one, impacting on the invadopodia-mediated ECM degradation and metastatic progression, deserves a deeper investigation.
