Schisandrin B exhibits potent anticancer activity in triple negative breast cancer by inhibiting STAT3

Xuanxuan Dai1, Changtian Yin1, Guilong Guo2

  • 1Department of Thyroid and Breast Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325035, China; Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325035, China.

Insights

Schisandrin B (Sch B) effectively inhibits aggressive triple-negative breast cancer (TNBC) growth by inducing cell death and halting tumor progression. This compound shows potent anti-tumor activity via STAT3 pathway inactivation.

Area of Science:

  • Oncology
  • Pharmacology
  • Biochemistry

Background:

  • Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype with limited treatment options.
  • Schisandrin B (Sch B) is a bioactive compound derived from Schisandra chinensis with potential therapeutic properties.

Purpose of the Study:

  • To investigate the anti-tumor effects of Schisandrin B (Sch B) on triple-negative breast cancer (TNBC).
  • To elucidate the underlying molecular mechanisms of Sch B's action against TNBC.

Main Methods:

  • In vitro studies using TNBC cell lines (MDA-MB-231, BT-549, MDA-MB-468).
  • In vivo studies using immunodeficient mice xenograft models.
  • Analysis of cell cycle arrest, apoptosis, migration, and colony formation.
  • Assessment of signal transducer and activator of transcription-3 (STAT3) phosphorylation and nuclear translocation.

Main Results:

  • Schisandrin B significantly inhibited TNBC cell proliferation, migration, and colony formation.
  • Sch B induced cell cycle arrest and promoted apoptotic cell death in TNBC cells.
  • The anti-tumor effects of Sch B were associated with the suppression of STAT3 phosphorylation and nuclear translocation.
  • Sch B demonstrated efficacy in preventing TNBC tumor growth in vivo.

Conclusions:

  • Schisandrin B exhibits potent anti-tumor activity against triple-negative breast cancer.
  • Sch B exerts its effects through the induction of cell cycle arrest, apoptosis, and inhibition of cell migration.
  • The novel mechanism involves the inactivation of the STAT3 signaling pathway, highlighting Sch B as a potential therapeutic agent for TNBC.

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