Discipline: Biological Sciences
Subcategory: Cancer Research
Natasha Bryant - J.F. Drake State Community and Technical College
Co-Author(s): Keira Davis, Alira Danaher, and Nathan Bowen, Clark Atlanta University Shamari Perkins, Spelman College, Atlanta, GA
Cell division in healthy, non-cancerous cells is tightly controlled. However, in cancer cells, the processes that control cell division are deregulated due to changes in the levels of proteins that regulate the cell cycle. Aberrant expression of regulatory proteins leads to increased growth and cell division within the tumor. We have identified the protein product of the gene ZIC2 as being a critical regulator of cell division in prostate cancer cells. We have shown that ZIC2 is aberrantly upregulated in prostate cancer. We have also shown that removing ZIC2 by gene editing leads to significant loss of cell division in prostate cancer cells. In this set of experiments, we will test the hypothesis that adding additional ZIC2 will increase cell division in prostate cancer cells. We will present results describing the growth characteristics and cell cycle analysis of a population of cells that have been engineered to express increased levels of ZIC2 relative to the parental cell population.
Funder Acknowledgement(s): This work funded in part by: 2G12MD007590 and LSAMP grant 1305041
Faculty Advisor: Nathan Bowen, email@example.com
Role: Shamari Perkins and I were Laboratory Assistants to Keira Davis and Alira Danaher. Our tasks included growing HEK cells, washing and feeding them, transfecting them with the ZIC2 gene, fixing cells with 70% ethanol alcohol and processing western blots to count the RNA during the cell cycle that the cells were frozen in.