Presentation Title
Effect of HDAC Inhibitor on DNA Methylation and Cell Cycle Regulation in Prostate Cancer
Location
Nova Southeastern University, Davie, Florida, USA
Format
Poster
Start Date
21-2-2020 8:30 AM
End Date
21-2-2020 4:00 PM
Abstract
Objective: Our study was aimed to analyse the expression of methyltransferase levels in LNCaP (prostate Cancer) cells during SAHA treatment. Background: Prostate cancer is the second leading cause of death in men after lung cancer in the US. Nearly 1 in 8 men will be diagnosed of prostate cancer in their lifetime, and the risk increases significantly once the men cross the age of 70. Recognizing ways to reduce the death of prostate cancer is therefore a top research priority. Epigenetic regulation of gene plays an important role in the controlling cell cycle and tumor growth in various cancers. Epigenetic changes generally occur through alterations in DNA and Histone modification such as acetylation, methylation, phosphorylation, and ubiquitination. SAHA (Suberoylanilide Hydroxamic Acid) is a broad spectram inhibitor of histone deacetylase (HDAC), which is used to modify the status of Histone Acetylation during cancer treatments. However, the impact of SAHA on methyltransferase levels or methylation status of DNA has not been studied in detail. Methods: LNCaP cells were cultured in complete RPMI-1640 growth medium and treated with SAHA (7.5 uM) for 24 hours. Western blot technique was used to analyze the expression levels of DNMT3A, SUV39H1, PRMT1, and p21. Results: Our experimental results have shown that SAHA treatment reduce the levels of the methyltransferase enzymes listed above. Furthermore, SAHA treatment increased the protein levels of p21, which is a CDKI (cyclin-dependent kinase inhibitor). Conclusion: Methylation is an important modification of DNA that can regulate gene expressions. Our results indicate that SAHA treatment, which is known to regulate histone acetylation, can impact the methylation status also through an indirect mechanism and allow for the control of transcription of tumor suppressor genes. Acknowledgement: This Research was supported by the Royal Dames of Cancer Research Inc., Ft. Lauderdale, Florida.
Effect of HDAC Inhibitor on DNA Methylation and Cell Cycle Regulation in Prostate Cancer
Nova Southeastern University, Davie, Florida, USA
Objective: Our study was aimed to analyse the expression of methyltransferase levels in LNCaP (prostate Cancer) cells during SAHA treatment. Background: Prostate cancer is the second leading cause of death in men after lung cancer in the US. Nearly 1 in 8 men will be diagnosed of prostate cancer in their lifetime, and the risk increases significantly once the men cross the age of 70. Recognizing ways to reduce the death of prostate cancer is therefore a top research priority. Epigenetic regulation of gene plays an important role in the controlling cell cycle and tumor growth in various cancers. Epigenetic changes generally occur through alterations in DNA and Histone modification such as acetylation, methylation, phosphorylation, and ubiquitination. SAHA (Suberoylanilide Hydroxamic Acid) is a broad spectram inhibitor of histone deacetylase (HDAC), which is used to modify the status of Histone Acetylation during cancer treatments. However, the impact of SAHA on methyltransferase levels or methylation status of DNA has not been studied in detail. Methods: LNCaP cells were cultured in complete RPMI-1640 growth medium and treated with SAHA (7.5 uM) for 24 hours. Western blot technique was used to analyze the expression levels of DNMT3A, SUV39H1, PRMT1, and p21. Results: Our experimental results have shown that SAHA treatment reduce the levels of the methyltransferase enzymes listed above. Furthermore, SAHA treatment increased the protein levels of p21, which is a CDKI (cyclin-dependent kinase inhibitor). Conclusion: Methylation is an important modification of DNA that can regulate gene expressions. Our results indicate that SAHA treatment, which is known to regulate histone acetylation, can impact the methylation status also through an indirect mechanism and allow for the control of transcription of tumor suppressor genes. Acknowledgement: This Research was supported by the Royal Dames of Cancer Research Inc., Ft. Lauderdale, Florida.