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Updated: Jun 26, 2026

Anticancer Efficacy of Photodynamic Therapy with Lung Cancer-Targeted Nanoparticles
08:03

Anticancer Efficacy of Photodynamic Therapy with Lung Cancer-Targeted Nanoparticles

Published on: December 1, 2016

Effects of Benzo[a]pyrene on Targeted Therapy Response and Platelet-Activating Factor-Receptor-Mediated Microvesicle

Riya Rawal1, Anita Thyagarajan1, Ravi P Sahu1

  • 1Department of Pharmacology and Toxicology, Boonshoft School of Medicine, Dayton, OH 45435, USA.

Medical Sciences (Basel, Switzerland)
|June 25, 2026
PubMed
Abstract

Insights

Environmental carcinogen Benzo[a]pyrene (BaP) increases non-small cell lung cancer (NSCLC) invasiveness via platelet-activating factor-receptor (PAFR) signaling. This modulation of NSCLC progression does not impact epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) efficacy.

Area of Science:

  • Oncology
  • Environmental Health
  • Molecular Biology

Background:

  • Non-small cell lung cancer (NSCLC) presents significant mortality due to invasive properties and therapy resistance.
  • Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are effective for EGFR-mutant NSCLC but face resistance.
  • Benzo[a]pyrene (BaP), a carcinogen in tobacco smoke and diet, is implicated in tumor progression, but its role in therapeutic response is unclear.

Purpose of the Study:

  • To investigate if platelet-activating factor-receptor (PAFR) activation mediates BaP-induced NSCLC progression.
  • To determine the effect of BaP on EGFR-TKI efficacy in NSCLC.
  • To explore PAFR as a potential therapeutic target in NSCLC.

Main Methods:

  • Assessed effects of BaP, PAFR agonist (CPAF), and EGFR-TKIs on NSCLC cell viability, proliferation, migration, anchorage-independent growth, and microvesicle particle (MVP) secretion.
  • Utilized a PAFR antagonist and an acid sphingomyelinase inhibitor to block BaP-induced effects.
  • Evaluated combined effects of BaP and EGFR-TKIs on NSCLC cell behavior.

Main Results:

  • BaP significantly enhanced NSCLC migration, growth, colony formation, and MVP release, mirroring CPAF effects.
  • These BaP-induced changes were abrogated by PAFR antagonist or acid sphingomyelinase inhibitor.
  • BaP did not significantly diminish the efficacy of EGFR-TKIs at tested concentrations.

Conclusions:

  • Environmental carcinogen BaP modulates NSCLC behavior via PAFR signaling.
  • PAFR pathway activation enhances NSCLC progression without compromising EGFR-TKI responsiveness.
  • PAFR represents a promising therapeutic target for managing NSCLC progression influenced by environmental factors.
Keywords:
benzo[a]pyreneepidermal growth factor receptormicrovesicle particlesnon-small cell lung cancerplatelet-activating factor-receptortargeted therapy

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