Effect of SAHA and UC2288 on Epithelial to Mesenchymal Transition in p53 Wild/Mutant Types of Lung Cancer Cells
Abstract
Lung cancer is one of the most lethal cancers and encompasses over 30% of cancer-related deaths among men and women globally. Cancer progression is marked by the downregulation of epithelial markers and upregulation of mesenchymal markers, which causes solid tumors to become malignant and increase their invasiveness and metastatic properties. The epithelial-mesenchymal transition (EMT) is facilitated through complex molecular pathways that include epigenetic and posttranslational modifications. In this regard, DNA as well as Histone methyltransferases are suspected to be involved within the EMT process. In our study, we analyzed the markers of EMT in H460 and HCC827 lung cancer cells using Histone Deacetylase inhibitor (HDACi) SAHA (Suberoylanilide Hydroxamic Acid) and p21 inhibitor (UC2288). The cells were treated with SAHA, UC2288, and combination for 24 hrs. Our western blot results have shown that SAHA treatment was able to increase E-cadherin, p21, p27 levels along with SNAI1 protein levels while decreasing the Aurora Kinase B and Vimentin expression levels. Our results provide a valuable information regarding the correlation between acetylation and methylation mechanisms, leading to the suppression of EMT following HDAC inhibition by SAHA. (This project was supported by The Royal Dames of Cancer Research Inc., Ft. Lauderdale, Florida).
Faculty Sponsors
Dr. Umamaheswari Natarajan, Dr. Thiagarajan Venkatesan, Dr. Appu Rathinavelu
Project Type
Event
Location
Alvin Sherman Library
Start Date
4-6-2021 12:00 PM
End Date
4-9-2021 12:00 PM
Effect of SAHA and UC2288 on Epithelial to Mesenchymal Transition in p53 Wild/Mutant Types of Lung Cancer Cells
Alvin Sherman Library
Lung cancer is one of the most lethal cancers and encompasses over 30% of cancer-related deaths among men and women globally. Cancer progression is marked by the downregulation of epithelial markers and upregulation of mesenchymal markers, which causes solid tumors to become malignant and increase their invasiveness and metastatic properties. The epithelial-mesenchymal transition (EMT) is facilitated through complex molecular pathways that include epigenetic and posttranslational modifications. In this regard, DNA as well as Histone methyltransferases are suspected to be involved within the EMT process. In our study, we analyzed the markers of EMT in H460 and HCC827 lung cancer cells using Histone Deacetylase inhibitor (HDACi) SAHA (Suberoylanilide Hydroxamic Acid) and p21 inhibitor (UC2288). The cells were treated with SAHA, UC2288, and combination for 24 hrs. Our western blot results have shown that SAHA treatment was able to increase E-cadherin, p21, p27 levels along with SNAI1 protein levels while decreasing the Aurora Kinase B and Vimentin expression levels. Our results provide a valuable information regarding the correlation between acetylation and methylation mechanisms, leading to the suppression of EMT following HDAC inhibition by SAHA. (This project was supported by The Royal Dames of Cancer Research Inc., Ft. Lauderdale, Florida).
