Event Title

Molecular Mechanisms of Cancer Stem Cell Creation via High Nitric Oxide Adaptation

Session Number

C13

Advisor(s)

James Radosevich, University of Illinois at Chicago

Location

A-129

Start Date

28-4-2016 2:00 PM

End Date

28-4-2016 2:25 PM

Disciplines

Biology

Abstract

For some time, it has been known tumors exhibit morphological and functional heterogeneity. Multiple theories have been proposed to address the cause of this, the most accepted of which is the hierarchy model, which states that biologically distinct cell classes compose tumors and only one has the ability to initiate tumor growth: the cancer stem cell (CSC) class. Today, however, the origin of these CSCs is unknown and under active research. One hypothesis has been that CSCs are actually results of the adaptation of cancer cells to nitric oxide in high amounts (HNO). We replicated this adaptive process, exposing five adenocarcinoma (AC) and five squamous cell carcinoma (SCC) cell lines to HNO levels. Using genechip analysis, we observed the changes in gene expression in the cancers from this adaptation process. With various bioinformatic tools, we determined which genes were commonly up and downregulated across the ACs, the SCCs, and both the ACs and SCCs. The significant down-regulation of pyruvate dehydrogenase across all cell lines suggests that HNO- adapted cells go through a nonstandard pathway of cellular respiration. Furthermore, HNO-adapted SCCs displayed increased ribosomal production and genomic instability typical of CSCs. Our results clearly support the idea that CSCs are created from HNO- adaptation.


Share

COinS
 
Apr 28th, 2:00 PM Apr 28th, 2:25 PM

Molecular Mechanisms of Cancer Stem Cell Creation via High Nitric Oxide Adaptation

A-129

For some time, it has been known tumors exhibit morphological and functional heterogeneity. Multiple theories have been proposed to address the cause of this, the most accepted of which is the hierarchy model, which states that biologically distinct cell classes compose tumors and only one has the ability to initiate tumor growth: the cancer stem cell (CSC) class. Today, however, the origin of these CSCs is unknown and under active research. One hypothesis has been that CSCs are actually results of the adaptation of cancer cells to nitric oxide in high amounts (HNO). We replicated this adaptive process, exposing five adenocarcinoma (AC) and five squamous cell carcinoma (SCC) cell lines to HNO levels. Using genechip analysis, we observed the changes in gene expression in the cancers from this adaptation process. With various bioinformatic tools, we determined which genes were commonly up and downregulated across the ACs, the SCCs, and both the ACs and SCCs. The significant down-regulation of pyruvate dehydrogenase across all cell lines suggests that HNO- adapted cells go through a nonstandard pathway of cellular respiration. Furthermore, HNO-adapted SCCs displayed increased ribosomal production and genomic instability typical of CSCs. Our results clearly support the idea that CSCs are created from HNO- adaptation.