Evidence map›Paper›PMID 42531287›Full record

ArticlePloS one2026

Verbascoside triggers apoptosis and ferroptosis in NSCLC by targeting BCAT2.

Ruijuan Li, Bin Li, Ping Wang

Abstract read
In one paragraph

Article in PloS one, 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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0citing papers in PubMed
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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Ruijuan LiDepartment of Respiratory Medicine, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.
Bin LiDepartment of Respiratory Medicine, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.
Ping WangDepartment of Respiratory Medicine, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.ORCID https://orcid.org/0009-0003-6236-8476

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe treatment of non-small cell lung cancer (NSCLC) has challenges such as drug resistance and recurrence. Concurrently, the induction of apoptosis and ferroptosis is a promising therapeutic strategy. This study aimed to investigate whether the natural product, verbascoside, induces apoptosis and ferroptosis in NSCLC cells by targeting BCAT2.

methodsBioinformatic analysis was used to predict the potential targets of verbascosides. Stable cell lines with BCAT2 knockdown and overexpression were constructed. The effects of verbascoside on NSCLC were evaluated in vitro and using a mouse xenograft model.

resultsBioinformatics screening and molecular docking identified BCAT2 as a potential target of verbascoside, with a significantly stronger binding energy (-7.8 kcal/mol) than another candidate, PARP1. In vitro and in vivo experiments confirmed that BCAT2 knockdown significantly inhibited NSCLC cell viability, induced apoptosis and ferroptosis, and induced mitochondrial damage. Conversely, BCAT2 overexpression produced opposite effects. Verbascoside treatment inhibited BCAT2 expression in a concentration-dependent manner, recapitulating the apoptotic, ferroptotic, and mitochondrial damage phenotypes induced by BCAT2 knockdown; however, BCAT2 overexpression significantly reversed these effects of verbascoside. In an animal model, treatment with verbascoside significantly suppressed tumor growth and activated apoptosis and ferroptosis in tumor tissues by downregulating BCAT2.

conclusionsVerbascoside can induce apoptosis and ferroptosis in NSCLC by directly targeting and inhibiting BCAT2, leading to mitochondrial dysfunction. This finding not only reveals BCAT2 as a novel target of verbascoside but also confirms its ability to induce apoptosis and ferroptosis in NSCLC cells.

Indexed as

ApoptosisCarcinoma, Non-Small-Cell LungFerroptosisGlucosidesLung NeoplasmsPhenolsTransaminasesAnimalsCell Line, TumorCell SurvivalGene Expression Regulation, NeoplasticHumansMiceMice, NudeMolecular Docking SimulationPolyphenolsacteosideGlucosidesPhenolsPolyphenolsTransaminases

Identifiers

PMID42531287
PMCPMC13422841

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.