Digesting the role of JAK-STAT and cytokine signaling in oral and gastric cancers
- Author(s)
- Ni,Yanhong; Low,Jun T; Silke,John; O’Reilly,Lorraine A;
- Journal Title
- Frontiers in Immunology
- Publication Type
- epub ahead of print
- Abstract
- When small proteins such as cytokines bind to their associated receptors on the plasma membrane, they can activate multiple internal signaling cascades allowing information from one cell to affect another. Frequently the signaling cascade leads to a change in gene expression that can affect cell functions such as proliferation, differentiation and homeostasis. The Janus kinase-signal transducer and activator of transcription (JAK-STAT) and the tumor necrosis factor receptor (TNFR) are the pivotal mechanisms employed for such communication. When deregulated, the JAK-STAT and the TNF receptor signaling pathways can induce chronic inflammatory phenotypes by promoting more cytokine production. Furthermore, these signaling pathways can promote replication, survival and metastasis of cancer cells. This review will summarize the essentials of the JAK/STAT and TNF signaling pathways and their regulation and the molecular mechanisms that lead to the dysregulation of the JAK-STAT pathway. The consequences of dysregulation, as ascertained from founding work in haematopoietic malignancies to more recent research in solid oral-gastrointestinal cancers, will also be discussed. Finally, this review will highlight the development and future of therapeutic applications which modulate the JAK-STAT or the TNF signaling pathways in cancers.
- Publisher
- Frontiers Media
- Keywords
- Cytokines,JAK,STAT,Oral,gastric,Cancer,PROTAC (proteolysis-targeting chimeric molecule),Immunotherapy,Inflammation,TNF
- Research Division(s)
- Inflammation
- Publisher's Version
- https://doi.org/10.3389/fimmu.2022.835997
- Open Access at Publisher's Site
https://doi.org/10.3389/fimmu.2022.835997- NHMRC Grants
- NHMRC/1107149, NHMRC/1195038,
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2022-07-04 08:57:00
Last Modified: 2022-07-04 09:06:40