Publications by authors named "G Mosialos"
TNF is a potent cytokine known for its involvement in physiology and pathology. In Rheumatoid Arthritis (RA), persistent TNF signals cause aberrant activation of synovial fibroblasts (SFs), the resident cells crucially involved in the inflammatory and destructive responses of the affected synovial membrane. However, the molecular switches that control the pathogenic activation of SFs remain poorly defined.
View Article and Find Full Text PDFBackground/aim: Breast cancer is a leading cause of cancer-related deaths among women. Down-regulation of the tumor suppressor gene Cyld in breast cancer has been linked to a poor prognosis. This study investigated the role of Cyld in breast cancer using conditional mutant mouse models carrying a Cyld mutation, which inactivates the deubiquitinating activity of its protein product CYLD in mammary epithelial cells.
View Article and Find Full Text PDFArticle Synopsis
- The text discusses the function of a tumor suppressor gene that codes for a deubiquitinating enzyme, which plays a key role in cancer-related signaling pathways and could also influence somatic cell reprogramming.
- Researchers investigated the impact of CYLD DUB deficiency in mouse embryonic fibroblasts (MEFs) during their reprogramming into induced pluripotent stem cells (iPSCs), finding that CYLD deficiency led to reduced reprogramming efficiency and altered early reprogramming processes.
- Proteome analysis showed that this deficiency disrupted critical cellular transitions and impacted pathways related to extracellular matrix organization and metabolism, establishing CYLD’s importance in the regulatory landscape of reprogramming and its implications for cancer research.
Downregulation of the cylindromatosis (CYLD) tumor suppressor has been associated with breast cancer development and progression. Here, we report a critical role for CYLD in maintaining the phenotype of mammary epithelial cells in vitro and in vivo. CYLD downregulation or inactivation induced an epithelial to mesenchymal transition of mammary epithelial cells that was dependent on the concomitant activation of the transcription factors Yes-associated protein (YAP)/transcriptional coactivator with PDZ-binding motif (TAZ) and transforming growth factor beta (TGF)signaling.
View Article and Find Full Text PDFBackground: Hepatocellular carcinoma (HCC) is a frequently diagnosed cancer and a leading cause of cancer-related death worldwide. Its rapid progression, combined with the limited treatment options at late stages, imposes the need for early detection and aggressive intervention. Based on the knowledge that hepatocarcinogenesis is significantly influenced by histone acetylation, we directed our search for novel HCC therapeutics among histone deacetylation inhibitors (HDACi).
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