Chemistry and Physics Faculty Proceedings, Presentations, Speeches, Lectures



Event Name/Location

Impact Oral Presentation / Impact Day and Honors Research Symposium / University of Illinois at Chicago / Chicago, Illinois

Event Name

Impact Day and Honors Research Symposium

Event Location

University of Illinois at Chicago / Chicago, IL

Document Type

Podium Presentation

Publication Date

Winter 11-22-2021


Hypothesis and Objective: Genes participating in the notch signaling pathway are influenced by exposure to high nitrous oxide (HNO) levels. Notch signaling pathway genes are responsible for regulating cell fate, differentiation, and apoptosis. Dysregulation of these genes can contribute to tumorigenesis. Alterations in the expression of these genes in MCF7 breast cancer cells could help determine the effects of the notch signaling pathway on tumorigenesis as a result of exposure to nitrous oxide.

Methods: Samples of cDNA from MCF7 and MCF7-HNO cells were used in DNA microarray analysis. Qualifying genes of interest provided a p value < .05. Differentially expressed genes (DEGs) were defined and categorized using the Gene Oncology Uniprot (GO) Molecular Function database. These cells were further analyzed using a proprietary bioinformatics analysis created by our laboratory.

Results: Exposure to HNO conditions significantly altered the expression of LLGL2 when compared to the parent cell lines. It was found that LLGL2 was upregulated (p < .05), while genes associated with LLGL2 were either upregulated (SCRIB, p < .01; GALE, p < .05; ZNF707, p < .05; RASSF7, p < .05) or downregulated (SLC16A1, p < .005).

Conclusions: The observed primary and secondary genes had various impacts on tumorigenesis in HNO cells. SCRIB and GALE were both upregulated. These genes are involved in cell differentiation and metabolic pathways, acting as tumor promoters. LLGL2, RASSF7, and ZNF707 were also upregulated. These genes are involved in organogenesis, apoptosis, and gene expression, and act as tumor suppressors. SLC16A1, a tumor promotor, was downregulated, suggesting it may not play a major role in HNO cells. Within the MCF7 cell line, LLGL2 appears to demonstrate dual roles in breast cancer following high NO exposure.

Funding: N/A

IRB and/or ACC Protocol #: N/A

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