Thesis

Is there an association between S1P signaling and the transcription factor Nrf2?

Creator
Rights statement
Awarding institution
  • University of Strathclyde
Date of award
  • 2016
Thesis identifier
  • T14327
Person Identifier (Local)
  • 201474657
Qualification Level
Qualification Name
Department, School or Faculty
Abstract
  • Nuclear factor-erythroid 2 [NF-E2]-related factor 2 (Nrf2) is a transcriptional activator that can offer protection to cells. By activating cytoprotective genes, Nrf2 can help cells to defend against DNA damage, electrophilic and oxidative stress. However, Nrf2 can also act as an oncogene. The upstream mutation leads to the Nrf2 overexpression and accumulation in the nucleus. In cancer development, overexpressed Nrf2 enhances the resistance of cancers to drugs, chemotherapy or radiotherapy. Sphingosine 1-phosphate is a biological lipid mediator that serves a pivotal function in physiological functions and pathophysiological conditions. Synthesized by sphingosine kinase, S1P regulates several cellular events through five sphingosine 1-phosphate receptors. S1P has been associated with poor prognosis in cancer, metastasis and chemotherapeutic resistance. Dysregulated Nrf2 and S1P are able to enhance chemotherapeutic resistance in cancer development. However, a direct association between Nrf2 and S1P has not been observed yet. The aim of this project was to examine whether there is a relationship between Nrf2 and S1P. Three cancer cell lines were employed and tested for the ability of S1P or sphingosine kinase inhibitors or short-chain ceramides to affect Nrf2. Although the work presented here does not support a relationship between Nrf2 and S1P, a direct connection between these two factors cannot yet be discounted. Based on their roles in cancer development, clarification of the potential connection between Nrf2 and S1P should be investigated further.
Resource Type
DOI
Alternative Title
  • Is there an association between S1P signalling and the transcription factor Nrf2?
Date Created
  • 2016
Former identifier
  • 9912524890602996

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