Some cancer cells form highly regulated structures, termed invadopodia, which mediate local, enzymatic degradation of extracellular matrix and facilitate cancer cell invasion and migration during metastatic progression. Understanding invadopodium formation and function in cancer cells is therefore an important strategy to find novel clinical approaches to interfere with metastasis. Invadopodia are F-actin-rich protrusions that form on the advancing edge of cells, supported by complex molecular interactions at the cell membrane. Invadopodia formation, structure, and function can be studied in vitro, using commonly cultured cancer cell lines and standard microscopic techniques. Here, these approaches are described in detail.
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http://dx.doi.org/10.1007/978-1-0716-3589-6_12 | DOI Listing |
J Am Heart Assoc
March 2025
Department of Biochemistry and Molecular Biology, College of Basic Medicine, Cardiovascular Medical Science Center, Key Laboratory of Vascular Biology of Hebei Province, Key Laboratory of Neural and Vascular Biology of Ministry of Education Hebei Medical University Shijiazhuang People's Republic of China.
Background: Phenotypic plasticity of vascular smooth muscle cells (VSMCs) is believed to be a key factor in neointima hyperplasia, which is the pathological basis of vascular remodeling diseases. LDHA (lactate dehydrogenase A) has been demonstrated to promote the proliferation and migration of VSMCs. However, the mechanism is still unclear.
View Article and Find Full Text PDFMol Cancer
February 2025
Department of Otolaryngology, Rainbow Blvd, University of Kansas Medical Center, 3901aq, Wahl Hall East 4031, Kansas, KS, 66160, USA.
Background: HNSCC presents a significant health challenge due to its high mortality resulting from treatment resistance and locoregional invasion into critical structures in the head and neck region. Understanding the invasion mechanisms of HNSCC has the potential to guide targeted therapies, improving patient survival. Previously, we demonstrated the involvement of doublecortin like kinase 1 (DCLK1) in regulating HNSCC cell invasion.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Laboratory of Pathological Anatomy and Immunohistochemistry, School of Dentistry, Federal University of Pará, Belém 66075-110, PA, Brazil.
The aim of this study was to verify whether the expression of proteins related to the formation of invadopodia, MT1-MMP, cortactin, Tks-4 and Tks-5 is associated with the degree of tumor invasiveness of different types of unicystic ameloblastomas. An immunohistochemical study was performed on 29 unicystic ameloblastoma (UA) samples, 9 conventional ameloblastoma (CAM) samples and 9 dental follicle (DF) samples. The potential for tumor invasiveness was assessed based on the immunoexpression of the following invadopodia-forming proteins: MT1-MMP, cortactin, Tks-4 and Tks5.
View Article and Find Full Text PDFAdv Protein Chem Struct Biol
January 2025
Department of Neurochemistry, National Institute of Mental Health and Neuro Sciences Hospital (NIMHANS), Institute of National Importance, Bangalore, Karnataka, India. Electronic address:
The neuronal cytoskeleton has remained a less explored area of research in establishing neuroprotection. HDAC6 has been studied with respect to many neurodegenerative diseases, especially AD. It exhibits the ability to interact with various cytoskeletal proteins and to promote migration in cells.
View Article and Find Full Text PDFMol Biol Cell
March 2025
Department of Biology, The Catholic University of America, Washington, DC 20064.
MAL2 (myelin and lymphocyte protein 2) and rab17 have been identified as hepatocellular carcinoma tumor suppressors. However, little is known how their functions in hepatic polarized protein sorting/trafficking translate into how they function in the epithelial-to-mesenchymal transition and/or the mesenchymal-to-epithelial transition in metastases. To investigate this, we expressed MAL2 and rab17 alone or together in hepatoma-derived Clone 9 cells (that lack endogenous MAL2 and rab17).
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