For the past months, I have attempted to collect data for my research study. Collecting data was not fairly simple, because it was a retrospective approach to collecting data, meaning that I didn’t get to follow a step by step protocol in order to get preliminary results. It took some time trying to digest all the research papers available on my topic of interest and if any data would be able to provide me with feasible information on genes correlated to C.elegans and Glioblastoma multiforme.
I was able to successfully screen over 30+ human GBM linked genes to see if they were orthologous to C.elegans. I successfully found 10 possible C.elegans genes that could be correlated to GBM in humans. I was able to do this with the help of two high-density genome platforms called Ensembl and Ortholist. It is satisfying to know that I was able to retrieve a few, but significant number of genes, although I feel that I need to look for more genes, and perform more screens on more potential GBM human genes. This will requite me to look through another vast number of papers which I am willing to do. This must be done, before any RNAi experiments can be performed to knock out any desired genes.
The title of my project is “Evaluating the function of genes implicated Glioblastoma multiforme (GBM) formation using C. elegans.” Caenorhabditis elegans (C.elegans) is an ideal organism for studying genes and proteins in humans on a genetic and molecular level. Humans have many genes in common with C.elegans, some of which may be associated with the development of cancer in humans. C. elegans is a valuble model system that we can study to get insights into how cell division is controlled and to understand how misregulation of cell division can ultimately lead to cancer. The goal of this study is to identify which genes present in C.elegans play a role in cancer development. In particular we are interested in genes that are known to play a role in the development of Glioblastoma multiforme (GBM), which is an aggressive form of brain cancer with very low rates of survival.
There are current and past studies that demonstrate there is a link between genetic variance and tumorigenesis (cancer development) in humans. These studies involved real-life and model cases where gene mutation resulted in the cancer. Furthermore, many studies implicate that the mutation of one specific gene is capable of disrupting other genes in the genome that have linked molecular/cellular interactions with that mutated gene. The changes in the genes may be so small, involving even a few proteins. This project will help elucidate and affirm how changes in genes could affect cell function that, in turn, could ultimately cause cancer.
First, I will identify which genes implicated in GBM development are also present in C. elegans. Then I will conduct RNA inference (RNAi) experiments in C. elegans, which will allow me to disrupt gene function and determine the function of those genes. After the RNAi experiments I will assess if cell division is disrupted by looking at embryo development. During embryo development, the cell must maintain the proper regulation of the cell cycle if not the embryo will not develop properly, which is similar to the errors that are seen in many cancers. These experiments will allow us to determine mechanistically what parts of the cell cycle are being affected and pinpoint the essential proteins that are linked to these abnormalities.