Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/157229
Title: Genome wide in-vivo functional genetic screen to identify novel modulators of Non-Alcoholic Fatty Liver Disease (NAFLD)
Authors: Lian, Ying
Keywords: Science::Biological sciences
Issue Date: 2022
Publisher: Nanyang Technological University
Source: Lian, Y. (2022). Genome wide in-vivo functional genetic screen to identify novel modulators of Non-Alcoholic Fatty Liver Disease (NAFLD). Final Year Project (FYP), Nanyang Technological University, Singapore. https://hdl.handle.net/10356/157229
Abstract: The rising incidence of non-alcoholic fatty liver disease (NAFLD) globally, specifically its advanced form, non-alcoholic steatohepatitis, is the representative cause of the increasing demand for liver transplantation. Characterised by excessive fat accumulation without clinically significant alcohol consumption, NAFLD remains a challenging healthcare burden due to the lack of therapeutics available. A distinctive phenomenon seen in NAFLD patients is the aberrant regenerative capability of the liver which limits compensation of lost liver mass leading to liver failure. Here, we identified five novel gene candidates that were postulated to regulate liver regeneration through the preliminary small hairpin RNAs (shRNA) mediated functional genetic screen. Effects caused by the shRNA-mediated knockdown of these candidates were validated through in vitro cell proliferation and migration assays. Downregulation of Targets 01, 02 and 03 robustly increased the proliferative and migratory capacity of hepatocytes. Conversely, downregulation of Slc35b3 significantly reduced cell growth and migration while function of Pcolce remains elusive due to poor efficacy of its shRNA. These results suggest that depletion of Targets 01, 02 and 03 can potentially be a viable treatment option to restore liver regenerative capacity in NAFLD patients and therefore demands further investigation to uncover new insights underlying NAFLD development and disease progression.
URI: https://hdl.handle.net/10356/157229
Fulltext Permission: restricted
Fulltext Availability: With Fulltext
Appears in Collections:SBS Student Reports (FYP/IA/PA/PI)

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