https://transhumanist.ru/index.php?action=history&feed=atom&title=SSX2 2026-06-10T12:20:11Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=SSX2&diff=4533&oldid=prev 2021-04-29T19:22:33Z

<p>Новая страница: «Protein SSX2 (Cancer/testis antigen 5.2) (CT5.2) (Synovial sarcoma, X breakpoint 2) (Tumor antigen HOM-MEL-40) [SSX2A] ==Publications== {{medline-entry |title=E...»</p> <p><b>Новая страница</b></p><div>Protein SSX2 (Cancer/testis antigen 5.2) (CT5.2) (Synovial sarcoma, X breakpoint 2) (Tumor antigen HOM-MEL-40) [SSX2A]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Ectopic expression of cancer/testis antigen [[SSX2]] induces DNA damage and promotes genomic instability.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/25363656<br /> |abstract=SSX cancer/testis antigens are frequently expressed in melanoma tumors and represent attractive targets for immunotherapy, but their role in melanoma tumorigenesis has remained elusive. Here, we investigated the cellular effects of [[SSX2]] expression. In A375 melanoma cells, [[SSX2]] expression resulted in an increased DNA content and enlargement of cell nuclei, suggestive of replication aberrations. The cells further displayed signs of DNA damage and genomic instability, associated with p53-mediated G1 cell cycle arrest and a late apoptotic response. These results suggest a model wherein [[SSX2]]-mediated replication stress translates into mitotic defects and genomic instability. Arrest of cell growth and induction of DNA double-strand breaks was also observed in MCF7 breast cancer cells in response to [[SSX2]] expression. Additionally, MCF7 cells with ectopic [[SSX2]] expression demonstrated typical signs of senescence (i.e. an irregular and enlarged cell shape, enhanced β-galactosidase activity and DNA double-strand breaks). Since replication defects, DNA damage and senescence are interconnected and well-documented effects of oncogene expression, we tested the oncogenic potential of [[SSX2]]. Importantly, knockdown of [[SSX2]] expression in melanoma cell lines demonstrated that [[SSX2]] supports the growth of melanoma cells. Our results reveal two important phenotypes of ectopic [[SSX2]] expression that may drive/support tumorigenesis: First, immediate induction of genomic instability, and second, long-term support of tumor cell growth.<br /> |mesh-terms=* Cell Line, Tumor<br /> * Cellular Senescence<br /> * DNA Breaks, Double-Stranded<br /> * G1 Phase Cell Cycle Checkpoints<br /> * Gene Expression Regulation, Neoplastic<br /> * Genomic Instability<br /> * Humans<br /> * Melanoma<br /> * Neoplasm Proteins<br /> * Repressor Proteins<br /> * Tumor Suppressor Protein p53<br /> |keywords=* Cancer/testis antigen<br /> * Genomic instability<br /> * Oncogene<br /> * SSX2<br /> * Senescence<br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5528659<br /> }}</div>

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