Investigation of the Role of G1p3 in Acetyl-CoA and Histone Acetylation Accumulation and Metabolic Reprogramming in Breast Cancer Cell Lines

Document Type

Thesis

Degree Name

Master of Science (MS)

Department

Biological and Environmental Sciences

Date of Award

9-1-2026

Abstract

Breast cancer is known as the most leading cause of cancer death in women worldwide. Preliminary studies have shown that metabolic reprogramming and epigenetic remodeling helps breast cancer cells in their metastatic progression and drug resistance. However, some of the molecular mechanisms are not completely understood. G1P3 (IFI6) – an interferon-induced gene located in mitochondria, and it has a crucial role in anti-apoptosis pathways and increasing mtROS levels in MCF-7 cell lines. Acetyl-CoA is also an important metabolic factor and studying the effects of interferon stimulated genes on it is important to understand breast cancer cells energy production and how it may influence. My study shows that the expression of G1P3 is associated with metabolic reprogramming in MCF-7 cells. Data analysis indicates that acetyl-CoA levels were significantly higher in MCF-7/G1P3 cells compared with MCF-7/Vector control cells and MCF-7 mutant strains. Based on our results, increased cellular metabolism is directly associated with a significant accumulation of histone acetylation in cells expressing the G1P3 gene. The results reveal that MCF-7/ Vector has been shown to have reduced levels of acetyl-CoA and histone acetylation than MCF-7 G1P3. This suggests that the overexpression of G1P3 may alter the metabolism of breast cancer cells in a way that increases acetyl-CoA which can leads to histone acetylation. Our results help us understand how the relation between the overexpression of G1P3 and Acetyl-CoA levels and Histone H3 acetylation levels is.

Advisor

Venu Cheriyath

Subject Categories

Biology | Life Sciences

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