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Verbascoside triggers apoptosis and ferroptosis in NSCLC by targeting BCAT2

Ruijuan Li1, Bin Li1, Ping Wang1

  • 1Department of Respiratory Medicine, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.

Plos One
|July 30, 2026
PubMed
Abstract

Insights

Verbascoside induces apoptosis and ferroptosis in non-small cell lung cancer (NSCLC) by targeting BCAT2. This natural compound offers a promising strategy against NSCLC drug resistance and recurrence.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Non-small cell lung cancer (NSCLC) presents treatment challenges including drug resistance and recurrence.
  • Inducing apoptosis and ferroptosis is a key therapeutic strategy for NSCLC.
  • Verbascoside, a natural product, is explored for its potential in NSCLC treatment.

Purpose of the Study:

  • To investigate if verbascoside induces apoptosis and ferroptosis in NSCLC cells.
  • To determine if BCAT2 is a molecular target of verbascoside in NSCLC.
  • To evaluate the therapeutic potential of verbascoside in NSCLC models.

Main Methods:

  • Bioinformatic analysis and molecular docking to identify verbascoside targets.
  • Construction of NSCLC cell lines with altered BCAT2 expression (knockdown and overexpression).
  • In vitro assays and a mouse xenograft model to assess verbascoside efficacy.

Main Results:

  • BCAT2 identified as a high-affinity target of verbascoside.
  • BCAT2 knockdown inhibited NSCLC viability and induced apoptosis, ferroptosis, and mitochondrial damage.
  • Verbascoside suppressed tumor growth and activated apoptosis/ferroptosis by downregulating BCAT2 in vivo.

Conclusions:

  • Verbascoside induces apoptosis and ferroptosis in NSCLC by directly targeting and inhibiting BCAT2.
  • BCAT2 is a novel therapeutic target for verbascoside in NSCLC treatment.
  • Verbascoside demonstrates potential as an anti-NSCLC agent via BCAT2-mediated mitochondrial dysfunction.

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