Evidence map›Paper›PMID 42474554›Full record

ArticleMolecular biology reports2026

Effects of stattic and vinblastine on apoptosis and fatty acid profile in A549 lung cancer cells.

Maryam Ashourpour, Jamal Mohammadian, Amir Mehdizadeh, Amir Ghorbanihaghjo

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Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

4 authors.

Maryam AshourpourDepartment of Clinical Biochemistry and Laboratory Sciences, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Jamal MohammadianDepartment of Clinical Biochemistry and Laboratory Sciences, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Amir MehdizadehHematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Amir GhorbanihaghjoBiotechnology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. ghorbaniamir@hotmail.com.

Funding

Biotechnology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran 72257
6 · The paper itself

Abstract

purposeNon-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.

methodsThe 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.

resultsThe 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.

conclusionThese findings suggest that the vinblastine-Stattic combination enhances anticancer activity in A549 cells and warrants further mechanistic and in vivo studies.

Indexed as

ApoptosisCarcinoma, Non-Small-Cell LungFatty AcidsLung NeoplasmsVinblastineA549 CellsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansSignal TransductionSTAT3 Transcription FactorFatty AcidsSTAT3 protein, humanSTAT3 Transcription FactorVinblastineApoptosisNon-small cell lung cancerSignal Transducer and Activator of Transcription 3StatticVinblastine

Identifiers

PMID42474554

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