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Updated: Feb 15, 2026

Methyl-binding DNA capture Sequencing for Patient Tissues
Published on: October 31, 2016
DNA methylation as mechanism of apoptotic resistance development in endometrial cancer patients
Veronika Fialkova1, Eva Vidomanova, Tomas Balharek
1Department of Medical Biochemistry, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, Martin, Slovakia. hatok@jfmed.uniba.sk.
Abstract:
DNA methylation is a significant epigenetic modification which plays a key role in regulation of gene expression and influences functional changes in endometrial tissue. Aberrant DNA methylation changes result in deregulation of important apoptotic proteins during endometrial carcinogenesis and apoptosis resistance development. Evading apoptosis is still a major problem in the successful treatment of endometrial cancer patients. The aim of our study was to examine the promoter DNA methylation changes in 22 apoptosis-associated genes in endometrioid endometrial cancer patients, precancerous lesions and healthy tissue from various normal menstrual cycle phases using a unique pre-designed methylation platform. We observed as the first a significant difference in promoter DNA methylation status in genes: BCL2L11 (p < 0.001), CIDEB (p < 0.03) and GADD45A (p < 0.05) during endometrial carcinogenesis and BIK gene (p < 0.03) in different phases of normal menstrual cycle. The results of our study indicate that deregulation of mitochondrial apoptotic pathway can considerably contributes to the apoptosis resistance development and may be helpful in identifying of new potent biomarkers in endometrial cancer.
Insights
DNA methylation changes in endometrial cancer affect apoptosis. Aberrant methylation in BCL2L11, CIDEB, GADD45A, and BIK genes may indicate new biomarkers for treatment resistance.
Area of Science:
- Epigenetics
- Molecular Biology
- Gynecologic Oncology
Background:
- DNA methylation is a critical epigenetic regulator of gene expression, impacting endometrial tissue function.
- Aberrant DNA methylation contributes to endometrial carcinogenesis by disrupting apoptotic protein regulation and promoting resistance to apoptosis.
- Resistance to apoptosis remains a significant challenge in treating endometrial cancer.
Purpose of the Study:
- To investigate promoter DNA methylation changes in 22 apoptosis-associated genes.
- To compare methylation patterns in endometrioid endometrial cancer, precancerous lesions, and healthy endometrial tissue across the menstrual cycle.
Main Methods:
- Utilized a pre-designed methylation platform for comprehensive analysis.
- Examined promoter DNA methylation status of 22 key apoptosis-associated genes.
- Included samples from endometrial cancer patients, precancerous lesions, and healthy controls.
Main Results:
- Identified significant differences in promoter DNA methylation for BCL2L11 (p < 0.001), CIDEB (p < 0.03), and GADD45A (p < 0.05) during endometrial carcinogenesis.
- Observed significant methylation changes in the BIK gene (p < 0.03) across different phases of the normal menstrual cycle.
- These findings highlight specific gene methylation alterations linked to cancer development and normal physiological processes.
Conclusions:
- Deregulation of the mitochondrial apoptotic pathway, indicated by altered DNA methylation, significantly contributes to apoptosis resistance in endometrial cancer.
- The identified methylation changes in apoptosis-associated genes may serve as potential biomarkers for endometrial cancer.
- Further research into these epigenetic modifications could lead to novel therapeutic strategies.
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