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Updated: Jun 20, 2026
Methyl-binding DNA capture Sequencing for Patient Tissues
Published on: October 31, 2016
AKAP12alpha is associated with promoter methylation in lung cancer
Ukhyun Jo1, Young Mi Whang, Han Kyeom Kim
1Department of Internal Medicine and Brain Korea 21 Project for Biomedical Science, Korea University College of Medicine, Seoul, Korea.
Purpose:
Promoter methylation is an important mechanism for silencing tumor-suppressor genes in cancer and it is a promising tool for the development of molecular biomarkers. The purpose of the present study was to investigate whether inactivation of the A Kinase Anchoring Protein 12 (AKAP12) gene is assoCiated with promoter methylation in lung cancer.
Materials And Methods:
The AKAP12 expression was examined by reverse transcription-polymerase chain reaction (RT-PCR) in ten lung cancer cell lines. The methylation status of the AKAP12alpha promoter was analyzed by performing bisulfite sequencing analysis in ten lung cancer cell lines, twenty four lung tissues and matched normal tissues.
Results:
The AKAP12alpha expression was reduced in 6 of 10 (60%) lung cancer cell lines, whereas the AKAP12beta expression was absent in 1 of 10 (10%) lung cancer cell lines. The AKAP12alpha expression was restored after treatment with the demethylating agent 5-aza-2'-deoxycytidine in three lung cancer cell lines. Methylation of CpG island 1 in the AKAP12alpha promoter was detected in 30% of the lung cancer cell lines, whereas methylation of CpG island 2 in the AKAP12alpha promoter was observed in the immortalized bronchial cell line and in all the lung cancer cell lines. In lung tumors, the CpG island 1 in the AKAP12alpha promoter was infrequently methylated. However, CpG island 2 in the AKAP12alpha promoter was highly methylated in lung tumors compared with the surrounding normal tissues, and this was statistically significant (p=0.0001).
Conclusion:
Our results suggest that inactivation of the AKAP12alpha expression is assoCiated with DNA methylation of the promoter region in lung cancer, and that AKAP12alpha may play an important role in lung cancer carcinogenesis.
Insights
Promoter methylation inactivates the AKAP12 gene in lung cancer. This study links A Kinase Anchoring Protein 12 (AKAP12) gene promoter methylation to its reduced expression, suggesting a role in lung cancer development.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- Promoter methylation is a key mechanism for silencing tumor-suppressor genes in cancer.
- Aberrant gene methylation serves as a potential biomarker for cancer detection and prognosis.
Purpose of the Study:
- To investigate the association between A Kinase Anchoring Protein 12 (AKAP12) gene promoter methylation and its inactivation in lung cancer.
- To explore the potential role of AKAP12 as a tumor suppressor in lung carcinogenesis.
Main Methods:
- Examined AKAP12 gene expression using reverse transcription-polymerase chain reaction (RT-PCR) in lung cancer cell lines.
- Analyzed AKAP12alpha promoter methylation status via bisulfite sequencing in lung cancer cell lines and tissues.
Main Results:
- Reduced AKAP12alpha expression was observed in 60% of lung cancer cell lines.
- AKAP12alpha promoter methylation was detected in lung cancer cell lines and highly prevalent in lung tumors compared to normal tissues (p=0.0001).
- Demethylating agent treatment restored AKAP12alpha expression in some cell lines, confirming methylation-induced silencing.
Conclusions:
- AKAP12 gene inactivation in lung cancer is associated with DNA promoter methylation.
- AKAP12alpha may function as a tumor suppressor, playing a significant role in lung cancer development.
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