Please use this identifier to cite or link to this item:
Title: Investigating the contribution of NF-κB2 to tumor proliferation and migration in glioblastoma multiforme
Authors: Goh, Zheng Cong
Keywords: DRNTU::Science::Biological sciences::Molecular biology
Issue Date: 2019
Abstract: Glioblastoma multiforme (GBM) is the deadliest type of astrocytoma whereby patients do not live over 2 years. The non-canonical nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling was reported to be hyperactivated in some human GBM cells and this is correlated with enhanced tumor proliferation and motility. NF-кB2 (p100/p52) is a transcription factor in the non-canonical NF-кB signaling pathway. However, how NF-кB2 contributes to GBM progression is poorly defined. Given that GBM is aggressive and invasive, this study aims to study the role of NF-кB2 in GBM proliferation and migration. This project focuses on characterizing endogenous NF-кB2 levels in different human GBM cell lines, overexpressing and knocking out p52, the active form nfкb2, in NF-кB2low and NF-кB2high cells respectively, and conducting functional assays to study the effects of NF-кB2 on GBM proliferation and migration. Our results show that p52 was successfully overexpressed in NF-кB2low LN18, D247 and LN382 human GBM cell lines, while p52 was knocked out in NF-кB2high LN444 and U87 cells. This study also demonstrates that NF-кB2 promotes GBM proliferation but has minimal effects on GBM migration. This calls for more investigations to confirm the role of non-canonical NF-кB signaling pathway in GBM.
Rights: Nanyang Technological University
Fulltext Permission: restricted
Fulltext Availability: With Fulltext
Appears in Collections:SBS Student Reports (FYP/IA/PA/PI)

Files in This Item:
File Description SizeFormat 
  Restricted Access
787.49 kBAdobe PDFView/Open

Page view(s)

Updated on Jun 18, 2021


Updated on Jun 18, 2021

Google ScholarTM


Items in DR-NTU are protected by copyright, with all rights reserved, unless otherwise indicated.