Research Publication Title

Treating HPV E6 Oncoprotein Induced Cervical Cancer Via CRISPR/Cas9 Genome Editing

Presenter Information

Garrett RogersFollow

Major

Biology

Faculty Mentor

Dr. Mike Gleason

Keywords

HPV, Cervical, Cancer, CRISPR, Editing, E6, Treatment, p53, Tumor

Abstract

Human papillomavirus (HPV) is the most common sexually transmitted disease in the United States and a common cause of cervical cancer. If a patient has HPV for an extended amount of time due to lack of vaccination, inadequate immune system response, or both, she is more susceptible to the development of cervical cancer. Affecting epithelial cells, the HPV E6 oncoprotein leads to the development of cervical cancer via the reduction of p53 tumor suppressor gene product. When functional, the p53 protein prevents genome mutation by one or more of three routes; growth arrest to facilitate DNA repair, autophagy, or apoptosis. A newly developed method of cervical cancer treatment employs the gene editing tool, CRISPR/Cas9, to introduce a double-strand break (DSB) within the viral oncogene inside infected cells. To accomplish this, a single guide RNA complementary to the E6 oncogene is used to guide the Cas9 nuclease. As Cas9 induced DSBs are usually repaired by non-homologous end joining (NHEJ), which almost always leads to a missense mutation being introduced during gene repair, the E6 expression in cervical cancer cells is “knocked-out”. Research described in this presentation indicates that this may be a viable route of treatment that could supplement, or potentially replace, the current treatments of surgery, radiation therapy, and chemotherapy that keep cervical cancer treatment harsh and drawn out.

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Treating HPV E6 Oncoprotein Induced Cervical Cancer Via CRISPR/Cas9 Genome Editing

Human papillomavirus (HPV) is the most common sexually transmitted disease in the United States and a common cause of cervical cancer. If a patient has HPV for an extended amount of time due to lack of vaccination, inadequate immune system response, or both, she is more susceptible to the development of cervical cancer. Affecting epithelial cells, the HPV E6 oncoprotein leads to the development of cervical cancer via the reduction of p53 tumor suppressor gene product. When functional, the p53 protein prevents genome mutation by one or more of three routes; growth arrest to facilitate DNA repair, autophagy, or apoptosis. A newly developed method of cervical cancer treatment employs the gene editing tool, CRISPR/Cas9, to introduce a double-strand break (DSB) within the viral oncogene inside infected cells. To accomplish this, a single guide RNA complementary to the E6 oncogene is used to guide the Cas9 nuclease. As Cas9 induced DSBs are usually repaired by non-homologous end joining (NHEJ), which almost always leads to a missense mutation being introduced during gene repair, the E6 expression in cervical cancer cells is “knocked-out”. Research described in this presentation indicates that this may be a viable route of treatment that could supplement, or potentially replace, the current treatments of surgery, radiation therapy, and chemotherapy that keep cervical cancer treatment harsh and drawn out.