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Caffeine-boosted silver nanoparticles target breast cancer cells by triggering oxidative stress, inflammation, and

Naief Dahran1, Mohamed S Othman2, Farah Mumtaz3

  • 1Department of Basic Medical Sciences, College of Medicine, University of Jeddah, Jeddah, 21959, Saudi Arabia.

Journal of Pharmaceutical Sciences
|April 25, 2025
PubMed

Insights

Caffeine-conjugated silver nanoparticles (Caf-AgNPs) show potent anticancer effects against breast cancer cells by inducing apoptosis and oxidative stress. This novel approach enhances efficacy while reducing toxicity to normal cells, offering a promising breast cancer intervention.

Area of Science:

  • Nanotechnology
  • Biomedical Engineering
  • Oncology

Background:

  • Breast cancer (BC) is a leading cause of cancer mortality in women globally.
  • Developing effective and less toxic breast cancer treatments remains a critical challenge.

Purpose of the Study:

  • To investigate the anticancer efficacy of caffeine-conjugated silver nanoparticles (Caf-AgNPs) against MDA-MB-231 breast cancer cells.
  • To compare the therapeutic effects of Caf-AgNPs with fluorouracil (5-FU) and assess their cytotoxicity on normal mouse liver (NBL) cells.

Main Methods:

  • Synthesis and characterization of caffeine-conjugated silver nanoparticles (Caf-AgNPs).
  • In vitro evaluation of Caf-AgNPs on MDA-MB-231 breast cancer cells and NBL cells.
  • Assessment of oxidative stress markers (ROS, MDA, GSH), inflammatory cytokines (COX-2, IL-1β, TNF-α), apoptosis-related proteins (Bax, Bcl-2, caspase-3), and cell cycle regulators (cyclin D1, CDK2).
  • Analysis of lactate dehydrogenase (LDH) release for membrane integrity.

Main Results:

  • Caf-AgNPs demonstrated significant anticancer activity against MDA-MB-231 cells, surpassing the efficacy of 5-FU.
  • Caf-AgNPs induced oxidative stress, apoptosis, and cell cycle arrest in cancer cells.
  • Conjugation of caffeine to silver nanoparticles (AgNPs) enhanced therapeutic efficacy and reduced cytotoxicity in normal liver cells.
  • Caf-AgNPs triggered apoptosis via mitochondrial pathways, evidenced by increased Bax, decreased Bcl-2, and caspase-3 activation.
  • Cellular membrane disruption was observed through elevated LDH leakage.

Conclusions:

  • Caf-AgNPs represent a promising therapeutic strategy for breast cancer intervention.
  • The multifaceted mechanisms of Caf-AgNPs include induction of oxidative stress, apoptosis, cell cycle arrest, and modulation of inflammatory responses.
  • Caf-AgNPs offer a potentially more effective and targeted approach to breast cancer treatment with reduced side effects.
Keywords:
Breast cancerCaffeineCell cycleMDA-MB 231 cell lineOxidative stressSilver nanoparticles

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