Submission Date

7-25-2025

Document Type

Paper

Department

Biology

Faculty Mentor

Ramesh Dasari

Comments

Presented during the 27th Annual Summer Fellows Symposium, July 18, 2025 at Ursinus College.

Attached as a supplemental file is a poster summarizing the research in this paper.

Project Description

Targeting glucose metabolism is an attractive strategy for cancer treatment, as cancer cells rely more heavily on glycolysis than oxidative phosphorylation, a phenomenon known as the Warburg Effect (Wang et al 2015). Reversing this metabolic reprogramming can impair cancer cell proliferation. NG52, a small-molecule inhibitor of PGK1, has been shown to effectively reverse the Warburg Effect and reduce cancer cell viability (Wycliffe et al. 2007). Paclitaxel, commonly Taxol, is a chemotherapeutic agent that disrupts mitotic spindle function, causing mitotic arrest and apoptosis (Markman et al 2005). In this study, we aimed to evaluate the individual and combined effects of NG52 and Paclitaxel on FaDu cells, a hypopharyngeal squamous carcinoma. We hypothesized that combining NG52 and Paclitaxel would produce a synergistic effect, enhancing cytotoxicity. FaDu cells were treated with varying concentrations of NG52 and Paclitaxel, alone and in combination, and cell activity inhibition was assessed using an MTT assay and an apoptosis and necrosis assay. IC₅₀ values were determined using CompuSyn software, and synergy was evaluated through the Chou-Talalay method. Results demonstrated that both agents decreased FaDu cell viability in a dose-dependent manner, yet their combination exhibited a combination index (CI) values equal to and greater than 1, indicating an additive and antagonistic interaction. These findings suggest that dual targeting of metabolic and mitotic pathways is not as effective for the treatment of hypopharyngeal cancers in comparison to single treatment by either of the two compounds.

Additional Files
Luke_N_Summer_Poster_25_ed_RD.pptx (2028 kB)
Research Poster
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