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Updated: Jan 6, 2026

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries
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Published on: January 22, 2019

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Saikosaponin D Modulates STAT3 and c-Myc Expression in MDA-MB-231 Cells: A Comprehensive In Silico and In Vitro Study

Bhuvaneshwari Deivendran1, Suryaa Manoharan1, Ekambaram Perumal2

  • 1Molecular Toxicology Laboratory, Department of Biotechnology, Bharathiar University, Coimbatore, 641046, India.

Applied Biochemistry and Biotechnology
|October 14, 2025
PubMed

Insights

Saikosaponin D (SSD) shows therapeutic potential against triple-negative breast cancer (TNBC). This compound effectively inhibits the STAT3/c-Myc pathway, reducing cancer cell viability and migration in preclinical studies.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Pharmacology

Background:

  • Triple-negative breast cancer (TNBC) is an aggressive subtype with limited therapeutic options.
  • The signal transducer and activator of transcription 3 (STAT3)/c-Myc pathway is frequently dysregulated in TNBC.
  • Saikosaponin D (SSD), derived from Bupleurum chinense, is a potential anticancer agent.

Purpose of the Study:

  • To investigate the therapeutic potential of saikosaponin D (SSD) against triple-negative breast cancer (TNBC).
  • To evaluate SSD's effect on the STAT3/c-Myc signaling pathway in MDA-MB-231 cells.
  • To explore SSD's mechanism of action through in silico and in vitro analyses.

Main Methods:

  • In silico docking and molecular dynamics simulations to predict SSD-protein interactions.
  • In vitro assays including cell viability, proliferation, migration, and apoptosis.
  • Gene expression analysis and Western blotting to assess pathway modulation.

Main Results:

  • SSD demonstrated significant binding affinity to STAT3 and c-Myc in silico.
  • In vitro, SSD reduced MDA-MB-231 cell viability (IC50 7.293 µM), proliferation, and migration.
  • SSD induced apoptosis, altered cell morphology, and dose-dependently inhibited STAT3 phosphorylation and c-Myc expression.

Conclusions:

  • Saikosaponin D exhibits promising therapeutic potential for TNBC.
  • SSD effectively targets the STAT3/c-Myc pathway, offering a novel therapeutic strategy.
  • These findings support further investigation of SSD for clinical development in TNBC treatment.
Keywords:
ApoptosisChemotherapyNecroptosisSTAT3Saikosaponin Dc-Myc

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