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Updated: Mar 8, 2026
Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors
Published on: August 5, 2022
An association between overexpression of DNA methyltransferase 3B4 and clear cell renal cell carcinoma
You Liu1, Liantao Sun1, Peter Fong2
1Biomedicine Research Center and Basic Medical College, Baotou Medical College, Inner Mongolia, PRC.
Abstract:
It is well known that abnormal DNA methylations occur frequently in kidney cancer. However, it remains unclear exactly which types of DNA methyltransferases (DNMT) contribute to the pathologies of kidney cancers. In order to determine the functions of DNA methyltransferase in kidney tumorigenesis on the molecular level, we examined the mRNA expression levels of DNMT1, DNMT3A, DNMT3B, and DNMT3B variants in renal cell carcinoma tissue. Both mRNA and protein levels of DNMT3B4, a splice variant of DNMT3B, were increased in renal cell carcinoma tissue compared with adjacent control tissues. Additionally, Alu elements and long interspersed nuclear elements (LINE-1) were hypomethylated in renal cell carcinoma tissue. Meanwhile, methylation of the promoter for RASSF1A, a tumor suppressor gene, was moderately increased in renal cell carcinoma tissue, while RASSF1A expression was decreased. Thus, our data suggest that the overexpression of DNMT3B4 may play an important role in human kidney tumorigenesis through chromosomal instability and methylation of RASSF1A.
Insights
Overexpression of DNA methyltransferase variant DNMT3B4 is linked to kidney cancer. This finding suggests DNMT3B4 contributes to kidney tumor development via chromosomal instability and RASSF1A gene methylation.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- Abnormal DNA methylation is common in kidney cancer.
- The specific DNA methyltransferases (DNMTs) involved in kidney cancer progression are not fully understood.
Purpose of the Study:
- To investigate the roles of DNMT1, DNMT3A, DNMT3B, and DNMT3B variants in kidney tumorigenesis.
- To determine the molecular mechanisms by which DNMTs contribute to renal cell carcinoma.
Main Methods:
- Examined mRNA expression of DNMT1, DNMT3A, DNMT3B, and DNMT3B variants in renal cell carcinoma tissue.
- Assessed protein levels of DNMT3B4.
- Analyzed methylation status of Alu elements, LINE-1, and the RASSF1A promoter in tumor tissues.
Main Results:
- Increased mRNA and protein levels of DNMT3B4 (a DNMT3B splice variant) were observed in renal cell carcinoma.
- Hypomethylation of repetitive elements (Alu and LINE-1) was detected in kidney tumors.
- Increased methylation and decreased expression of the tumor suppressor gene RASSF1A were found in renal cell carcinoma tissue.
Conclusions:
- Overexpression of DNMT3B4 may drive kidney tumorigenesis.
- DNMT3B4 could contribute to tumor development by inducing chromosomal instability.
- DNMT3B4 may promote kidney cancer through aberrant methylation of the RASSF1A tumor suppressor gene.
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