Signaling molecules have important roles in many cellular functions, but because these pathways are incredibly complex, the exact mechanisms often remain unknown. One signaling molecule, protein kinase C alpha (PKCα), is involved in cell proliferation and is expressed at high levels in many cancers. Interestingly, its activity as a tumor promoter or tumor suppressor varies depending on the cell type for reasons not yet fully understood. This study aimed to investigate the role of PKCα in cell proliferation in order to better understand its function as a signaling molecule. To assess this, a knockout line was generated using CRISPR-Cas9 and human embryonic kidney (HEK) cells. After confirmation of knockout, proliferation studies were conducted on untreated knockout and wild-type cells and upon addition of 0-0.5 μg/mL of PMA and 0-5 μg/mL of sphingosine-1-phosphate to induce proliferation. Our results indicate that compared with wild-type cells, untreated PKCα knockout cells exhibited reduced proliferation and had high percentages of cell death when treated with proliferative agents. This supports the hypothesis that PKCα knockout reduces proliferation in human embryonic kidney cells and suggests that PKCα has an important role in normal cell function in a tumor-promoting context.
Kuntz, Emma J.
"Exploring the Effects of Protein Kinase C Alpha Gene Knockout on the Proliferation of Human Embryonic Kidney Cells,"
ELAIA: Vol. 2
, Article 10.
Available at: https://digitalcommons.olivet.edu/elaia/vol2/iss1/10