adam-15 [Neurosurgery Wiki]

This page is read only. You can view the source, but not change it. Ask your administrator if you think this is wrong.
ADAM-15, or a disintegrin and metalloproteinase 15, is a member of the ADAM family of proteins that are involved in cell signaling, adhesion, and proteolysis. ADAM-15 is a transmembrane protein that is expressed in various tissues, including the brain, heart, lungs, and kidneys.

Research has implicated ADAM-15 in various biological processes, including cell proliferation, migration, and invasion. ADAM-15 has also been suggested to play a role in the development and progression of various diseases, including cancer, cardiovascular disease, and inflammatory disorders.

In cancer, ADAM-15 has been shown to promote tumor growth, angiogebnesis, and metastasis. ADAM-15 has also been suggested as a potential therapeutic target for cancer treatment. In cardiovascular disease, ADAM-15 has been implicated in the regulation of vascular smooth muscle cell function and the development of atherosclerosis. In inflammatory disorders, ADAM-15 has been suggested to play a role in the regulation of immune cell function and the development of autoimmune diseases.

Further research is needed to fully understand the role of ADAM-15 in various biological processes and diseases. However, the diverse functions of ADAM-15 and its potential as a therapeutic target make it an interesting target for future research.
----
The purpose of a study by Piperi et al. was to investigate the clinical significance of [[SSADH]] expression in human [[glioma]]s. Using [[public single-cell RNA-sequencing data]] from glioma surgical resections, Piperi et al. initially grouped [[cancer cell]]s according to [[ALDH5A1]] (Aldehyde dehydrogenase 5 family member A1) expression, which encodes [[SSADH]]. [[Gene ontology]] enrichment analysis of genes differentially expressed between cancer cells expressing high or low levels of ALDH5A1, highlighted enrichment in genes implicated in the cell [[morphogenesis]] and motility. In glioblastoma cell lines, ALDH5A1 knockdown inhibited cell proliferation, induced [[apoptosis]], and reduced their migratory potential. This was accompanied by a reduction in the [[mRNA]] levels of the adherens junction molecule [[ADAM-15]] and deregulation in the expression of EMT biomarkers, with increased [[CDH1]] and decreased [[vimentin]] [[mRNA]] levels. Evaluation of SSADH expression in a cohort of 95 gliomas using [[immunohistochemistry]] showed that [[SSADH]] expression was significantly elevated in cancer tissues compared to normal brain tissues, without any significant correlation with clinicopathological characteristics. In summary, data show that SSADH is upregulated in [[glioma]]  irrespective of the histological grade, and its expression sustains [[glioma cell motility]]
((Piperi C, Saurty-Seerunghen MS, Levidou G, Sepsa A, Trigka EA, Klonou A, Markouli M, Strepkos D, Spyropoulou A, Kanakoglou DS, Lakiotaki E, Karatrasoglou EA, Boviatsis E, El-Habr EA, Korkolopoulou P. Glioma Cells Expressing High Levels of ALDH5A1 Exhibit Enhanced Migration Transcriptional Signature in Patient Tumors. Neurotherapeutics. 2023 Mar 28. doi: 10.1007/s13311-023-01354-8. Epub ahead of print. PMID: 36976494.))