Date of Award

5-2025

Document Type

Honors Thesis

Degree Name

Bachelor of Science

Department

Biological Science

Advisor/Committee Chair

Jason I. Herschkowitz

Major

Biology

Committee Member

Thomas Begley

Abstract

Breast cancer encompasses a diverse range of diseases characterized by the uncontrolled proliferation of cells within the mammary gland. This condition results in an accumulation of a large number of genetic mutations within an individual, altering the complex internal signaling system of a cell. Millions of women are affected by breast cancer, which remains a significant threat despite medical advancements. Ductal carcinoma in situ (DCIS) acts as a precursor to invasive ductal carcinoma (IDC), however, not all cases progress to invasive cancer. Triple-negative breast cancer (TNBC) is identified to be one aggressive subtype of IDC, where the cells lack sufficient levels of progesterone receptors, estrogen receptors, and HER2 proteins. According to numerous studies, super-enhancers not only promote gene transcription but also result in super-enhancer long noncoding RNAs (SE-lncRNA) by transcribing themselves, playing an important role in tumor progression. These SE-lncRNAs can interact with associated enhancer regions and influence the expression of neighboring genes. Even though DCIS does not always lead to breast cancer, the current approach to DCIS treatment remains an aggressive course of therapy, resulting in over-treatment. It is therefore essential to identify functional elements that drive the transition from DCIS to IDC, to differentiate the treatments for indolent and aggressive forms of the disease. Studying the role of these SE-lncRNAs can aid in advancing therapeutic techniques. Here, we knockdown two specific SE-lncRNAs, TFAP2A–AS1 and RP11-379F4.4 in the MCF10A-CA1 (CA1) cell line to observe its effect on its neighboring protein-coding genes, TFAP2A and RARRES1, respectively.

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