Authors
Maryam Ashourpour, Jamal Mohammadian, Amir Mehdizadeh, Amir Ghorbanihaghjo
Published in
Molecular biology reports. Volume 53. Issue 1. Jul 20, 2026. Epub Jul 20, 2026.
Abstract
Non-small cell lung cancer (NSCLC) is among the most lethal cancers globally, partly due to dysregulated STAT3 signaling, which is related to tumor growth. Combination strategies involving STAT3 inhibitors with chemotherapeutic agents may improve therapeutic efficacy. Therefore, the current study assessed the effects of Stattic (a STAT3 inhibitor) in combination with vinblastine (a microtubule-destabilizing agent) against A549 lung cancer cells.
The antiproliferative effect was examined using MTT assay, apoptosis by Annexin V-FITC/PI and DAPI staining, cell cycle distribution by flow cytometry, and cell migration by wound-healing assay. Molecular changes in apoptosis-related genes were evaluated by qRT-PCR, and alterations in fatty acid profiles were analyzed via gas-liquid chromatography.
The IC₅₀ values for vinblastine and Stattic were 11.3 nM and 1.8 µM, respectively. Co-treatment of Stattic with vinblastine significantly inhibited cell migration, increased the percentage of apoptotic cells, elevated the mRNA expression of the pro-apoptotic gene Bak, and reduced the expression of anti-apoptotic genes Bcl-2 and Mcl-1. In addition, vinblastine treatment elevated saturated fatty acid levels, while Stattic increased monounsaturated fatty acid levels; their combination produced an intermediate lipid profile, indicating treatment-associated changes in cellular fatty acid composition.
These findings suggest that the vinblastine-Stattic combination enhances anticancer activity in A549 cells and warrants further mechanistic and in vivo studies.
PMID:
42474554
Bibliographic data and abstract were imported from PubMed on 20 Jul 2026.
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