Disruption of epidermal growth factor receptor signaling and cytoskeletal dynamics by mebendazole and gefitinib synergistically impairs paracrine cytokine signaling in non-small cell lung cancer and triple-negative breast cancer Cell lines.

ABSTRACT:

Background

Aberrant paracrine cytokine signaling and dysregulated signal transduction are critical drivers of tumor progression and therapeutic resistance in aggressive cancers such as non-small cell lung cancer and triple-negative breast cancer. This study aimed to explore a dual-targeting strategy using mebendazole, a repurposed anti-parasitic agent known to disrupt microtubules, in combination with gefitinib, an epidermal growth factor receptor tyrosine kinase inhibitor. The objective was to assess the combinatorial impact on cell viability and key regulatory pathways involved in inflammation, mitotic control, and nuclear transport.

Methods

Human lung adenocarcinoma (A549) and triple-negative breast cancer (MDA-MB-231) cell lines were treated with mebendazole, gefitinib,

SUBMITTER: El-Tanani M 

PROVIDER: S-EPMC12707669 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature