DNA Damage Response to High Nitric Oxide Exposure in A549 Cancer Cells
Session Number
Project ID: MEDH 34
Advisor(s)
Dr. James Radosevich; University of Illinois at Chicago, College of Dentistry
Discipline
Medical and Health Sciences
Start Date
22-4-2020 10:05 AM
End Date
22-4-2020 10:20 AM
Abstract
A comparative analysis was conducted between high NO adapted (HNO) A549 cells and parental A549 cells to reveal significantly altered gene expression levels as a result of adaptation to NO. Previous reports by this laboratory demonstrated increased NO overexpression by tumor cells lead to further tumor progression. HNO cells are characteristically more aggressive and resistant the genes: ATF2, EME1, MSH2, MUS81, RAD9A, TIPIN, XPC, could potentially be involved in the resulting phenotype developed by HNO cells. These genes are essential to the intra-S DNA Damage checkpoint, a mitotic cell cycle checkpoint that slows DNA synthesis in response to DNA damage by the prevention of new origin firing and the stabilization of slow replication fork progression. Previous studies have shown that Nitric Oxide is overexpressed in human tumors and produces a poor outcome. In high Nitric Oxide adapted (HNO) cells, signal transduction in response to DNA damage is altered. We focused on determining what genes are associated with the response to DNA damage from high nitric oxide exposure. Understanding the genetic profile of aggressive tumors could lead to a change in how therapeutic approaches will be defined.
DNA Damage Response to High Nitric Oxide Exposure in A549 Cancer Cells
A comparative analysis was conducted between high NO adapted (HNO) A549 cells and parental A549 cells to reveal significantly altered gene expression levels as a result of adaptation to NO. Previous reports by this laboratory demonstrated increased NO overexpression by tumor cells lead to further tumor progression. HNO cells are characteristically more aggressive and resistant the genes: ATF2, EME1, MSH2, MUS81, RAD9A, TIPIN, XPC, could potentially be involved in the resulting phenotype developed by HNO cells. These genes are essential to the intra-S DNA Damage checkpoint, a mitotic cell cycle checkpoint that slows DNA synthesis in response to DNA damage by the prevention of new origin firing and the stabilization of slow replication fork progression. Previous studies have shown that Nitric Oxide is overexpressed in human tumors and produces a poor outcome. In high Nitric Oxide adapted (HNO) cells, signal transduction in response to DNA damage is altered. We focused on determining what genes are associated with the response to DNA damage from high nitric oxide exposure. Understanding the genetic profile of aggressive tumors could lead to a change in how therapeutic approaches will be defined.