AI Article Synopsis
- Human SSX genes are a family of 6 known members, with SSX1, 2, and 4 implicated in the t(X;18) translocation linked to synovial sarcomas.
- Four of these genes (SSX1, 2, 4, and 5) are expressed in certain tumors and testis, making them typical cancer-testis antigens and associated with antibodies in cancer patients.
- Researchers identified three additional SSX genes (SSX7, 8, and 9) through genomic analysis, while SSX6 was fully sequenced, revealing that most SSX genes are located on chromosome X, with specific expression patterns in normal and cancerous tissues.
Article Abstract
Human SSX genes comprise a gene family with 6 known members. SSX1, 2 and 4 have been found to be involved in the t(X;18) translocation characteristically found in all synovial sarcomas. Four (SSX1, 2, 4 and 5) are known to be expressed in a subset of tumors and testis, and anti-SSX antibodies have been found in sera from cancer patients. SSX antigens are thus typical cancer-testis (CT) antigens. To identify additional SSX family members, we isolated and characterized human genomic clones homologous to a prototype SSX cDNA. We also searched public databases for sequences similar to SSX. This identified 3 additional SSX genes, SSX7, 8, 9, and also completed the sequence of the formerly partially defined SSX6 gene. In addition to these novel SSX genes, several SSX pseudogenes were identified. With the exception of 1 pseudogene, all SSX genomic SSX sequences map to chromosome X. Among normal tissues, SSX7 mRNA was present only in testis, whereas SSX6, 8 and 9 were not detected in any normal tissue. SSX6 and 7 were expressed in 1 of 9 melanoma cell lines tested, whereas SSX8 and 9 expression was not detected in any tumor tissue or cell lines tested. SSX1, 2, 4 and 5 mRNA expression can be induced in cell lines by 5-aza-2-deoxycytidine or Trichostatin A. These agents also induce SSX6, but not SSX3, 7, 8 or 9 in the tumor cell lines tested, indicating that mechanisms other than methylation or histone acetylation may be responsible for the repressed state of some SSX genes.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1002/ijc.10634 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
SS18-SSX drives TYK2 expression to activate STAT3/Bcl2 axis, facilitating apoptosis evasion and advancing synovial sarcoma progression.
Cell Biol Toxicol
December 2024
The First Affiliated Hospital of Jinan University, Guangzhou, 510630, China.
Synovial sarcoma (SS) is a rare soft tissue sarcoma characterized by high-grade malignancy and poor prognosis. Preliminary research indicates that apoptosis evasion is a key factor in SS progression, primarily attributed to the overexpression of anti-apoptotic genes. However, the mechanisms underlying this phenomenon are still not fully understood.
View Article and Find Full Text PDFEZH2 inhibition sensitizes retinoic acid-driven senescence in synovial sarcoma.
Cell Death Dis
November 2024
Department of Microbiology, Tumor and Cell Biology (MTC), Biomedicum, Karolinska Institutet, SE-171 65, Stockholm, Sweden.
Synovial sarcoma (SS) is driven by a unique t(18;X) chromosomal translocation resulting in expression of the SS18-SSX fusion oncoprotein, a transcriptional regulator with both activating and repressing functions. However, the manner in which SS18-SSX contributes to the development of SS is not entirely known. Here, we show that SS18-SSX drives the expression of Preferentially Expressed Antigen in Melanoma (PRAME), which is highly expressed in SS but whose function remains poorly understood.
View Article and Find Full Text PDFCondensate remodeling reorganizes innate SS18 in synovial sarcomagenesis.
Oncogenesis
October 2024
Laboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
SS18-SSX onco-fusion protein formed through aberrant chromosomal translocation t (X, 18; p11, q11), is the hallmark and plays a critical role in synovial sarcomagenesis. The recent works indicated that both the pathological SS18-SSX tumorigenic fusion and the corresponding intrinsic physiological SS18 protein can form condensates but appear to have disparate properties. The underlying regulatory mechanism and the consequent biological significance remain largely unknown.
View Article and Find Full Text PDFSUMO2 Inhibition Reverses Aberrant Epigenetic Rewiring Driven by Synovial Sarcoma Fusion Oncoproteins and Impairs Sarcomagenesis.
bioRxiv
September 2024
Cancer Genome and Epigenetics Program, National Cancer Institute-Designated Cancer Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037, USA.
Article Synopsis
- * Researchers found that a fusion protein called SS18-SSX drives the cancer's growth, and by analyzing cancer data, they identified that SUMO2 is a key gene that SySa cells rely on to survive.
- * The drug TAK-981, which inhibits SUMO2, was shown to effectively stop SySa cell growth and reverse harmful gene activities tied to the cancer, suggesting it could be a promising targeted treatment option as it is already in clinical trials for other cancers.
Combination of HDAC and FYN inhibitors in synovial sarcoma treatment.
Front Cell Dev Biol
July 2024
Department of Biology, Jacksonville State University, Jacksonville, AL, United States.
The SS18-SSX fusion protein is an oncogenic driver in synovial sarcoma. At the molecular level, SS18-SSX functions as both an activator and a repressor to coordinate transcription of different genes responsible for tumorigenesis. Here, we identify the proto-oncogene as a new SS18-SSX target gene and examine its relation to synovial sarcoma therapy.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!