| Description |
Cancer metastasis is one of the distinguishing traits that make the disease difficult to treat. The steps of tumor invasion are similar to a process called epithelial to mesenchymal transition (EMT). Retinoic acid (RA) is shown to inhibit EMT and may cause an increased transcription of the gene, skiB. This gene may play a role in EMT regulation through RA synthesis activation. Thus, this study used in-situ hybridizations labeling RNA expression of the gene, skiB, and morpholinos to knock down expression. These experiments were performed in the presence of TP-0903, a multi-kinase inhibitor that increases retinoic acid biosynthesis. Results show increased expression, while knocking down the gene provides inconclusive results. By exploring further details on the molecular mechanisms of EMT, cancer treatment can be improved by creating better targeted therapies. Moreover, future research will involve investigating other genes that may be associated with EMT and increased synthesis of RA. |
