Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/65300
Title: Identification of AHR and hypoxia co-regulated immune target genes as potential factors of inflammation-driven oncogenesis
Authors: Zaiden, Norazean
Keywords: DRNTU::Science::Biological sciences::Molecular biology
Issue Date: 2015
Source: Zaiden, N. (2015). Identification of AHR and hypoxia co-regulated immune target genes as potential factors of inflammation-driven oncogenesis. Master's thesis, Nanyang Technological University, Singapore.
Abstract: The transcription factors AHR and HIFs dimerize with the common co-activator ARNT during adaptive responses to xenobiotic exposure and oxygen tension. This cross-talk may subsequently modulate inflammation and/or physiological adaptation via immune cellular survival and maturation. Dysregulation of AHR and HIF pathways can cause chronic inflammation leading to oncogenesis, thus we hypothesized that AHR and hypoxia signaling co-operate in potentiating inflammation-driven oncogenesis. To address this, we analyzed AHR-mediated transcriptional responses in three frequently xenobiotic-exposed study models (murine liver, human keratinocytes, human intestinal epithelial cells), especially in the intestine, where AHR and hypoxia signaling constantly co-exist. Although AHR signaling is evolutionary conserved, we find that the AHR mediates diverse responses in a cell type- and species-dependent manner. Concurrent activation with hypoxia signaling in intestinal cells indicate a promotion of chronic inflammation through down-regulation of numerous anti-inflammatory target genes, and up-regulation of pro-inflammatory genes such as PTGS2, GZMB, and MMP1.
URI: http://hdl.handle.net/10356/65300
Fulltext Permission: restricted
Fulltext Availability: With Fulltext
Appears in Collections:SBS Theses

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