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Published on: April 2, 2020
Shank-associated RH domain interactor signaling in tumorigenesis
Chong Zeng1, Dan Xiong2, Ketao Zhang3
1Medical Research Center, Shunde Hospital, Southern Medical University, The First People's Hospital of Shunde, Foshan, Guangdong 528308, P.R. China.
Abstract:
Shank-associated RH domain interactor (SHARPIN) is a component of the linear ubiquitin chain activation complex, which is essential for p53 signaling and inflammation. Previous studies have demonstrated that SHARPIN functions in tumor cell survival, growth, invasion and tumorigenesis. These functions include the regulation of p53 proteins via poly-ubiquitination, interaction with a type II protein arginine methyltransferase 5 in melanoma cells, modulating ras-associated protein-1 through p38 and c-Jun N-terminal kinases/c-Jun signaling, and mediating phosphoinositide 3-kinase/AKT signaling via phosphatase and tensin homologue deleted on chromosome 10. Hence, SHARPIN not only participates in the inflammatory response but also serves a critical role in tumor cells. The present review summarizes the biological functions of the absence or presence of SHARPIN with regard to activating the canonical NF-κB signaling pathway and the effects on p53 and other signaling pathways for the modulation of tumorigenesis. Therefore, this review provides insight into the underlying role and mechanisms of SHARPIN in tumorigenesis, as well as its potential application in cancer therapy.
Insights
Shank-associated RH domain interactor (SHARPIN) is crucial for inflammation and p53 signaling. This review explores SHARPIN
Area of Science:
- Molecular Biology
- Cell Biology
- Cancer Research
Background:
- SHARPIN is a key component of the linear ubiquitin chain activation complex.
- SHARPIN plays essential roles in p53 signaling and inflammatory responses.
- Previous research indicates SHARPIN's involvement in tumor cell survival, growth, invasion, and tumorigenesis.
Purpose of the Study:
- To review the biological functions of SHARPIN in the context of its presence or absence.
- To elucidate SHARPIN's role in activating the canonical NF-κB signaling pathway.
- To summarize SHARPIN's effects on p53 and other signaling pathways in modulating tumorigenesis.
Main Methods:
- Literature review of existing studies on SHARPIN.
- Analysis of SHARPIN's interactions with various signaling molecules and pathways.
- Synthesis of data on SHARPIN's impact on tumorigenesis.
Main Results:
- SHARPIN regulates p53 protein poly-ubiquitination.
- SHARPIN interacts with protein arginine methyltransferase 5 in melanoma cells.
- SHARPIN modulates ras-associated protein-1 and mediates phosphoinositide 3-kinase/AKT signaling.
Conclusions:
- SHARPIN is critical for both inflammatory responses and tumor cell functions.
- Understanding SHARPIN's mechanisms in tumorigenesis is vital.
- SHARPIN presents potential as a therapeutic target in cancer treatment.
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