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<p>Triple-negative breast cancer (TNBC) is a highly aggressive subtype of breast cancer. This study investigates the therapeutic potential of saikosaponin D (SSD), an active compound from <i>Bupleurum chinense</i>, in targeting the signal transducer and activator of transcription 3 (STAT3)/c-Myc signaling pathway in MDA-MB-231 cells. In silico analysis utilizing AutoDock Vina and HawkDock server predicted SSD’s binding affinity with pivotal proteins such as STAT3 and c-Myc, uncovering a complex network of interactions. Molecular dynamics simulation using Schrödinger forecasted the stability of SSD with these target proteins. In vitro studies encompass a range of assays to evaluate the impact of SSD on MDA-MB-231 cells. SSD significantly decreased cell viability (IC<sub>50</sub> -7.293&#xa0;µM) and inhibited cell proliferation as evidenced by colony formation assay. Wound healing assay showed that SSD&#xa0;reduced the&#xa0;migratory potential of MDA-MB-231 cells. SSD induces cell morphological changes, confirmed through DAPI staining, scanning electron microscopy, and phalloidin staining. Live/Dead assay provides evidence that SSD causes decreased viability and increased apoptosis in MDA-MB-231 cells. Gene expression studies revealed that 4&#xa0;µM SSD significantly impacted apoptotic and necroptotic markers. Finally, Western blotting results&#xa0;revealed that SSD effectively inhibits STAT3 phosphorylation and suppresses c-Myc in a dose-dependent manner. In summary, both in silico and in vitro findings underscore SSD’s potential as a therapeutic agent against TNBC, highlighting its ability to modulate the STAT3/c-Myc signaling pathway and offering valuable insights for further clinical development.</p>

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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

  • 期刊论文

  • 发表日期：

    2025年10月14日

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  • Bhuvaneshwari Deivendran,
  • Suryaa Manoharan,
  • Ekambaram Perumal

摘要

Triple-negative breast cancer (TNBC) is a highly aggressive subtype of breast cancer. This study investigates the therapeutic potential of saikosaponin D (SSD), an active compound from Bupleurum chinense, in targeting the signal transducer and activator of transcription 3 (STAT3)/c-Myc signaling pathway in MDA-MB-231 cells. In silico analysis utilizing AutoDock Vina and HawkDock server predicted SSD’s binding affinity with pivotal proteins such as STAT3 and c-Myc, uncovering a complex network of interactions. Molecular dynamics simulation using Schrödinger forecasted the stability of SSD with these target proteins. In vitro studies encompass a range of assays to evaluate the impact of SSD on MDA-MB-231 cells. SSD significantly decreased cell viability (IC50 -7.293 µM) and inhibited cell proliferation as evidenced by colony formation assay. Wound healing assay showed that SSD reduced the migratory potential of MDA-MB-231 cells. SSD induces cell morphological changes, confirmed through DAPI staining, scanning electron microscopy, and phalloidin staining. Live/Dead assay provides evidence that SSD causes decreased viability and increased apoptosis in MDA-MB-231 cells. Gene expression studies revealed that 4 µM SSD significantly impacted apoptotic and necroptotic markers. Finally, Western blotting results revealed that SSD effectively inhibits STAT3 phosphorylation and suppresses c-Myc in a dose-dependent manner. In summary, both in silico and in vitro findings underscore SSD’s potential as a therapeutic agent against TNBC, highlighting its ability to modulate the STAT3/c-Myc signaling pathway and offering valuable insights for further clinical development.