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Reprogramming the oncogenic response: SET protein as a potential therapeutic target in cancer
Man-Hsin Hung1,2, Kuen-Feng Chen3
1a Division of Medical Oncology, Department of Oncology , Taipei Veterans General Hospital , Taipei , Taiwan.
Introduction:
SET is a multitask oncoprotein that promotes the initiation and progression of cancer. Overexpression of SET has been characterized as being tumor-specific and is associated with adverse clinical outcomes in many different human malignant diseases. Notably, SET has been shown to promote the development of therapeutic resistance in cancer cells. Area covered: In this review, we summarized the currently available evidence relating to the oncogenic roles, biological functions and clinical relevance of SET protein in cancer. The anti-cancer effects of three different SET antagonists undergoing preclinical investigation are also discussed. Expert opinion: Emerging evidence supports the critical role of SET in regulating various different cancer hallmarks. Targeting the SET-associated protein interfaces may be a potential anti-cancer strategy for future development. However, more studies are required to clarify the best strategy to combine SET antagonists with other anti-cancer treatments and to explore possible biomarkers that predict responsiveness.
Insights
The SET protein drives cancer initiation, progression, and therapeutic resistance. Targeting SET and its interactions offers a promising anti-cancer strategy, though further research is needed for optimal clinical application.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- The SET protein is an oncoprotein implicated in cancer initiation and progression.
- SET overexpression is tumor-specific and linked to poor clinical outcomes across various malignancies.
- SET contributes to the development of therapeutic resistance in cancer cells.
Purpose of the Study:
- To review the oncogenic roles, biological functions, and clinical relevance of SET protein in cancer.
- To discuss the anti-cancer effects of preclinical SET antagonists.
Main Methods:
- Literature review of existing evidence on SET protein in cancer.
- Summary of preclinical investigations into SET antagonists.
Main Results:
- SET plays a critical role in regulating diverse cancer hallmarks.
- Emerging evidence highlights SET's involvement in therapeutic resistance.
- Three SET antagonists show potential anti-cancer effects in preclinical studies.
Conclusions:
- Targeting SET-associated protein interfaces is a potential anti-cancer strategy.
- Further research is required to optimize combination therapies involving SET antagonists.
- Identifying biomarkers for predicting responsiveness to SET-targeted treatments is crucial.
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