Targeted Delivery of Rapamycin via Epidermal Growth Factor Receptors in Pancreatic Cancer Cells Inhibits Cell Proliferation and Induces Apoptosis

Authors

• Adeolu S. Oluremi, University of Arkansas at Little Rock
• Christofer Baldwin, University of Arkansas, Fayetteville
• Nickolas L. Gustavision, University of Arkansas, Fayetteville
• Mujeebat Bashiru, University of Arkansas at Little Rock
• Adeniyi Nsiah Oyebade, University of Arkansas at Little Rock
• Noureen Siraj, University of Arkansas at Little Rock
• Raj Raghavendra Rao, University of Arkansas, FayettevilleFollow
• N. Ali, University of Arkansas at Little RockFollow

Document Type

Article

Publication Date

7-29-2025

Keywords

Gold Nanoparticles, Drug-Delivery, Silver Nanoparticles, Oxidative Stress, Cost-Effectiveness, Cytotoxicity, Therapy, Death, Generation, Adenocarcinoma

Abstract

Pancreatic cancer (PC) is aggressive and deadly; most PC cells overexpress an epidermal growth factor receptor (EGFR). EGFR-targeting peptide (GE11) was conjugated to gold nanoparticles (AuNPs) for delivering rapamycin (Rap), an mTOR inhibitor that reduces proliferation and induces apoptosis. Biophysical techniques confirmed the conjugation. Rap loading efficiency was 41.5%, with sustained release at a lower pH. Conjugates showed higher uptake in PANC-1 cells than unmodified AuNPs. It also inhibited proliferation and induced apoptosis via pathways involving reactive oxygen species, mitochondrial damage, and caspase activation. This approach represents a promising nanoparticle-based therapeutic strategy targeting PC cells, utilizing GE11-EGFR interactions to minimize toxicity and enhance the efficacy of the therapeutic drug.

Comments

Web of Science

ACS

Citation

Adeolu S. Oluremi, Christofer Baldwin, Nickolas Gustavison, Mujeebat Bashiru, Adeniyi Oyebade, Noureen Siraj, Raj Raghavendra Rao, Nawab Ali; Targeted Delivery of Rapamycin via Epidermal Growth Factor Receptors in Pancreatic Cancer Cells Inhibits Cell Proliferation and Induces Apoptosis. ACS Omega 29 July 2025; 10 (29): 31762–31775. https://doi.org/10.1021/acsomega.5c02820

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