Access Type

Open Access

Presentation Type

Oral Presentation

Start Date

April 2017

End Date

April 2017

Department

Biology

Abstract

Lung cancer accounts for more deaths per year than any other form of cancer, resulting in a total of 158,000 deaths per year in the U.S. Non-small cell lung cancer (NSCLC) is diagnosed in greater than 224,000 Americans every year. Methylation and subsequent downregulation of certain genes has been directly linked to the uncontrolled growth of NSCLC cells. Natural killer (NK) cells are key innate immune cells responsible for apoptosis of cells with incorrect genetic code. It is believed that one component of uncontrolled NSCLC growth is due to the NK cells’ inability to detect errors within NSCLC cells. Perhaps an error occurs within these cells to prevent apoptosis; one such gene potentially responsible for this error is GATA-2 which is transcribed into a protein called GATA binding protein 2. I have hypothesized that GATA-2 methylation is occurring via c-Myc, a known methylator in NSCLC. In order to test my hypothesis, small-interfering RNA (siRNA) will be used to silence c-Myc. Bisulfite sequencing and methylation-specific PCR will be used to assay for GATA-2 methylation, and western blotting can be used to look for changes in c-Myc or GATA-2 protein. Any changes will be compared to non-silenced NSCLC cells.

Faculty Mentor

Allison Jablonski

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C-MYC’s role on Methylation of the GATA-2 gene in Non-Small Cell Lung Carcinoma

Lung cancer accounts for more deaths per year than any other form of cancer, resulting in a total of 158,000 deaths per year in the U.S. Non-small cell lung cancer (NSCLC) is diagnosed in greater than 224,000 Americans every year. Methylation and subsequent downregulation of certain genes has been directly linked to the uncontrolled growth of NSCLC cells. Natural killer (NK) cells are key innate immune cells responsible for apoptosis of cells with incorrect genetic code. It is believed that one component of uncontrolled NSCLC growth is due to the NK cells’ inability to detect errors within NSCLC cells. Perhaps an error occurs within these cells to prevent apoptosis; one such gene potentially responsible for this error is GATA-2 which is transcribed into a protein called GATA binding protein 2. I have hypothesized that GATA-2 methylation is occurring via c-Myc, a known methylator in NSCLC. In order to test my hypothesis, small-interfering RNA (siRNA) will be used to silence c-Myc. Bisulfite sequencing and methylation-specific PCR will be used to assay for GATA-2 methylation, and western blotting can be used to look for changes in c-Myc or GATA-2 protein. Any changes will be compared to non-silenced NSCLC cells.