Standing

Undergraduate

Type of Proposal

Oral Research Presentation

Faculty

Faculty of Science

Faculty Sponsor

Dr. Lisa A. Porter

Abstract/Description of Original Work

Liver cancer is the fourth leading cause of cancer-related deaths worldwide, standing at an estimation of 800,000 deaths annually. Among the various subtypes, hepatocellular carcinoma (HCC) is the most common primary liver malignancy. HCC is known to develop through a series of genetic and epigenetic alterations of proto-oncogenes and tumour suppressor genes in the liver environment. These changes ultimately lead to the malignant transformation of hepatocytes, the primary cells of the liver. Various HCC drivers are known to cause disruption of cellular pathways and promote tumour formation. Importantly, several cell cycle mediators cause misregulation, thereby stimulating tumour formation and progression. The cyclin-like protein Spy1, promotes cell cycle progression and overrides apoptosis. Recent reports have detected increased levels of Spy1 in human HCC, which directly correlates to severity of the disease and poor prognosis. We hypothesize that Spy1 plays a critical role along with hepatocellular carcinoma drivers to advance tumour development.  We will test the essentiality of Spy1 on HCC development by first investigating potential gRNAs to use for Spy1 knockout in vivo in the liver, for hydrodynamic tail vein injections in wildtype mice. Simultaneously, in vitro testing of HCC cells (HepG2) will study the importance of Spy1 in HCC cell characteristics in combination with HCC drivers such as c-myc, p53, and 𝛽-catenin. This project will assist in understanding the essentiality of Spy1 in HCC, which may reveal insight into the molecular mechanism of the tumour suppressors and proto-oncogenes connected with this subset of liver cancer.

Availability

March 29 (1-3 pm), March 31 (2-3 pm), April 1 (12-1 pm)

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The Essentiality of Spy1 in Cooperation with Hepatocellular Carcinoma Drivers to Promote Tumour Formation

Liver cancer is the fourth leading cause of cancer-related deaths worldwide, standing at an estimation of 800,000 deaths annually. Among the various subtypes, hepatocellular carcinoma (HCC) is the most common primary liver malignancy. HCC is known to develop through a series of genetic and epigenetic alterations of proto-oncogenes and tumour suppressor genes in the liver environment. These changes ultimately lead to the malignant transformation of hepatocytes, the primary cells of the liver. Various HCC drivers are known to cause disruption of cellular pathways and promote tumour formation. Importantly, several cell cycle mediators cause misregulation, thereby stimulating tumour formation and progression. The cyclin-like protein Spy1, promotes cell cycle progression and overrides apoptosis. Recent reports have detected increased levels of Spy1 in human HCC, which directly correlates to severity of the disease and poor prognosis. We hypothesize that Spy1 plays a critical role along with hepatocellular carcinoma drivers to advance tumour development.  We will test the essentiality of Spy1 on HCC development by first investigating potential gRNAs to use for Spy1 knockout in vivo in the liver, for hydrodynamic tail vein injections in wildtype mice. Simultaneously, in vitro testing of HCC cells (HepG2) will study the importance of Spy1 in HCC cell characteristics in combination with HCC drivers such as c-myc, p53, and 𝛽-catenin. This project will assist in understanding the essentiality of Spy1 in HCC, which may reveal insight into the molecular mechanism of the tumour suppressors and proto-oncogenes connected with this subset of liver cancer.