Targeting Cancer Stem Cell Survival in Triple-Negative Breast Cancer Through Bacterial Effector-Mediated NF-κB Inhibition

Neil Bhatia; Karan Mediratta; Lisheng Wang

doi:10.18192/osurj.v5i2.8053

Targeting Cancer Stem Cell Survival in Triple-Negative Breast Cancer Through Bacterial Effector-Mediated NF-κB Inhibition

Authors

Neil Bhatia University of Ottawa, Ottawa, ON, Canada
Karan Mediratta University of Ottawa, Ottawa, ON, Canada
Lisheng Wang University of Ottawa, Ottawa, ON, Canada

DOI:

https://doi.org/10.18192/osurj.v5i2.8053

Abstract

Triple-Negative Breast Cancer (TNBC) is an aggressive breast cancer subtype characterized by the absence of estrogen, progesterone, and HER2 receptors, resulting in limited responsiveness to standard therapies. Chemotherapy is the primary treatment and induces initial tumour regression; however, TNBC frequently recurs due to the persistence of Cancer Stem Cells (CSCs), a subpopulation capable of self-renewal, tumour regeneration, and therapeutic resistance. A central driver of CSC survival is Nuclear Factor Kappa B (NF-κB), a transcriptional regulator that promotes inflammation, anti-apoptotic signalling, and resistance to cytotoxic stress. In TNBC, NF-κB signalling is chronically active, reinforcing CSC-mediated chemoresistance and disease relapse. Current treatment strategies do not effectively eliminate CSCs or directly suppress NF-κB signalling, highlighting a critical therapeutic gap. This study
aims to evaluate whether a panel of bacterial effector proteins can be repurposed as targeted molecular tools to inhibit NF-κB signalling in TNBC. These effectors were selected based on their ability to disrupt NF-κB activation. TNBC models were engineered to enable controlled expression of these effectors across a variety of cell lines. NF-κB activity was assessed using reverse transcription quantitative polymerase chain reaction (RT-qPCR) and flow cytometry, while flow cytometry was also used to evaluate apoptosis and CSC marker expression. This work provides mechanistic insight into targeting CSC-driven resistance pathways and informs the development of more precise therapeutic strategies for aggressive TNBC.

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Published

2026-06-17

Issue

Vol. 5 No. 2 (2026)

Section

Undergraduate Science Research Opportunity Abstracts

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