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Updated: Jul 14, 2026

Application of MassSQUIRM for Quantitative Measurements of Lysine Demethylase Activity
Published on: March 11, 2012
Lysine methyltransferase SETD7 in cancer: functions, molecular mechanisms and therapeutic implications
Bo-Wen Zhang1, Ting Huang1, Yi-Fan Yang1
1Department of Basic Medicine, School of Medicine, Jiangsu University, Zhenjiang, 212013, China.
Abstract:
Since its discovery as a histone methyltransferase, SETD7 has been implicated in many signaling pathways and carcinogenesis. SETD7 catalyzes the methylation of histone H3 and non-histone proteins, regulating their translation, stability and activity. SETD7 is frequently abnormally expressed and has a significant influence on cell proliferation, invasion, autophagy and immune response. As cancer is a complex disease, an outstanding concept in cancer biology is the "hallmarks of cancer". In this review, we focus on the involvement of SETD7 in the hallmarks of cancer, describing its functions and underlying mechanisms in detail. Additionally, we discuss non-coding RNAs and chemical inhibitors targeting SETD7, highlighting the potential and importance of SETD7 in cancer therapy.
Insights
SETD7, a histone methyltransferase, plays a key role in cancer development by influencing cell processes. Targeting SETD7 offers promising therapeutic strategies for cancer treatment.
Area of Science:
- Biochemistry
- Molecular Biology
- Cancer Biology
Background:
- SETD7 is a histone methyltransferase involved in numerous signaling pathways and carcinogenesis.
- It regulates gene expression and protein activity through methylation of histone and non-histone proteins.
- Abnormal SETD7 expression is linked to key cancer processes like proliferation, invasion, autophagy, and immune response.
Purpose of the Study:
- To review the involvement of SETD7 in the hallmarks of cancer.
- To detail the functions and mechanisms of SETD7 in cancer.
- To discuss therapeutic strategies targeting SETD7.
Main Methods:
- Literature review focusing on SETD7 functions in cancer.
- Analysis of SETD7's role in cancer hallmarks.
- Exploration of non-coding RNAs and chemical inhibitors targeting SETD7.
Main Results:
- SETD7 influences multiple hallmarks of cancer, including sustained proliferative signaling, evading growth suppressors, resisting cell death, and enabling replicative immortality.
- SETD7's aberrant expression is a significant driver of cancer progression.
- Non-coding RNAs and small molecule inhibitors show potential for targeting SETD7 in cancer therapy.
Conclusions:
- SETD7 is a critical regulator in cancer development and progression.
- Understanding SETD7's mechanisms provides insights into cancer biology.
- Targeting SETD7 presents a promising avenue for novel cancer therapeutics.
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