Excerpt from: Rab Vesicle Trafficking is Required for Ras Mediated Proliferation in Cancer Cells

A Scripted Freelance Writer Writing Sample

The Ras superfamily consists of over 150 members including the well-known: H-Ras, K-Ras and N-Ras. We propose to target Ras related proliferation in cancer cells by inhibiting Rab vesicle formation. H-Ras, K-Ras and N-Ras are carcinogenic; activating mutations in Ras signaling are generally associated with increased proliferation and survival in cancer cells. Ras is mutated in up to 30% of all human cancers and represents an early survival mutation in cancer cells. Vesicle-bound Ras is trafficked to the plasma membrane, which facilitates interaction between Raf, and effector proteins. Previously, farnsesylation inhibitors, (FTIs) and GTP binding agonists of Ras have been tested as potential pharmacological inhibitors of Ras signaling. However, both drug types have proven ineffective in-vivo. Therefore, there are currently no effective pharmacological treatments to target Ras signaling. However, unpublished data from our lab has identified co-localization of Ras and Rab proteins, in vesicles. Rab proteins are associated with vesicle budding, and endosome development. Rab activity is driven by GTP binding and geranylgeranylation. Non-geranylgeranylated Rab is cytosolic, and does not facilitate endosome formation or vesicle trafficking. We propose that by targeting the Rab specific geranylgeranylation via Rab-specific geranylgeranyl transferase II, we will inhibit Ras associated proliferation. We will pursue this hypothesis by testing three objectives. First, we will produce and test Rab-geranylgeranyl transferase (RGGT)-shRNA to target Rab specific geranylgeranyl transferase. Second, we will illustrate the effect of RGGT knockdown on a downstream signaling target of Ras, specifically pERK levels. Finally, we will measure the direct effect of RGGT knockdown on Ras mediated cellular proliferation. Our results conclude that RGGT-shRNA is a potential target of Ras mediated tumor proliferation.


Esme G

San Francisco, California, United States •

I am passionate about the future of scientific research and science writing. I aspire to promote a better understanding of the scientific process, and current scientific discoveries to the public, while promoting the direction of scientific inquiry. I previously completed my Master's Thesis in Biomedical Research, with an emphasis in Cancer and Genetics. I completed my research at Dr. Lawrence Goldfinger's lab at Temple Medical School in Philadelphia. My independent research project was primarily centered on cellular signaling and iso-forms of Ras protein. Ras mutations are prevalent in an estimated 20-30% of all human cancers. I am a passionate, enthusiastic writer. I have contributed publications online science blogs, my university newspaper and literary magazine. I also maintained a travel blog, and can provide technical, casual ...

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