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Regulation of gene expression in human cancers by TRIM24
Srikanth Appikonda1, Kaushik N Thakkar2, Michelle Craig Barton2
1Department of Epigenetics and Molecular Carcinogenesis, Center for Cancer Epigenetics, Houston, TX 77030, USA.
Abstract:
Tripartite Motif-containing protein 24 (TRIM24) functions as an E3 ligase targeting p53 for ubiquitination, a histone 'reader' that interacts with a specific signature of histone post-translational modifications and a co-regulator of nuclear receptor-regulated transcription. Although mouse models of Trim24 depletion suggest that TRIM24 may be a liver-specific tumor suppressor, several studies show that human TRIM24 is an oncogene when aberrantly over expressed. This review focuses on the mechanisms of TRIM24 functions in oncogenesis and metabolic reprogramming, which underlie recent interest in therapeutic targeting of aberrant TRIM24 in human cancers.
Insights
Tripartite Motif-containing protein 24 (TRIM24) has dual roles in cancer. While mouse studies suggest it
Area of Science:
- Molecular Biology
- Cancer Research
- Epigenetics
Background:
- Tripartite Motif-containing protein 24 (TRIM24) exhibits multifaceted functions, including E3 ligase activity against p53, histone modification recognition, and nuclear receptor co-regulation.
- Contrasting evidence exists regarding TRIM24's role in tumorigenesis; mouse models indicate tumor suppression, whereas human studies identify it as an oncogene upon overexpression.
Purpose of the Study:
- To review the mechanistic roles of TRIM24 in oncogenesis.
- To explore TRIM24's involvement in metabolic reprogramming within cancer.
- To highlight the therapeutic potential of targeting aberrant TRIM24 in human cancers.
Main Methods:
- Literature review of existing studies on TRIM24.
- Analysis of TRIM24's molecular functions (E3 ligase, histone reader, co-regulator).
- Synthesis of data on TRIM24's oncogenic and metabolic roles.
Main Results:
- TRIM24's dual function as a potential tumor suppressor (mouse models) and oncogene (human cancers) is highlighted.
- Mechanisms linking TRIM24 to cancer development, including p53 regulation and epigenetic modifications, are discussed.
- TRIM24's contribution to metabolic reprogramming in cancer cells is explored.
Conclusions:
- Aberrant TRIM24 expression is implicated in human oncogenesis and metabolic reprogramming.
- TRIM24 represents a promising therapeutic target for various human cancers.