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Author Spotlight: Investigating the Potential of Chinese Herbal Medicinal Active Dioscin in Treating IgA Nephropathy
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Dioscin suppresses epithelial-mesenchymal transition in gastric cancer by upregulating Cx43 to inhibit the

Yu Kou1, Rentao Zhu2, Feng Gu1

  • 1School of Traditional Chinese Medicine, Faculty of Medicine, Yangzhou University, Yangzhou, 225009, PR China; NATCM Key Laboratory of Syndrome Differentiation and Treatment of Gastric Cancer, Yangzhou, 225009, PR China.

Phytomedicine : International Journal of Phytotherapy and Phytopharmacology
|December 7, 2025
PubMed
Abstract

Insights

Dioscin, a natural compound, inhibits gastric cancer metastasis by upregulating connexin 43 (Cx43) and enhancing its function, thereby suppressing the VEGFA/PI3K/AKT/mTOR pathway. This study reveals Cx43

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Connexin 43 (Cx43) and its gap junctions (Cx43-GJs) are implicated in cancer metastasis.
  • Dioscin demonstrates anticancer properties, but its mechanism in gastric cancer (GC) regarding Cx43 is unclear.

Purpose of the Study:

  • To investigate the anti-metastatic effects of dioscin on gastric cancer cells.
  • To elucidate the underlying molecular mechanisms involving Cx43 and associated signaling pathways.

Main Methods:

  • Integrated network pharmacology, molecular docking, and dynamics simulations.
  • Utilized in vitro (cell lines, mutants, knockdown) and in vivo (xenograft) models.
  • Assessed proliferation, invasion, migration, epithelial-mesenchymal transition (EMT), and signaling via Western blot, immunofluorescence, and co-immunoprecipitation.

Main Results:

  • Identified the VEGFA/PI3K/AKT/mTOR pathway as crucial in GC malignancy.
  • Dioscin suppressed this pathway by upregulating Cx43 and enhancing gap junction function.
  • Demonstrated that functional Cx43 is essential for dioscin's anti-metastatic efficacy through a dual-barrier mechanism.

Conclusions:

  • Dioscin inhibits GC metastasis by suppressing the VEGFA/PI3K/AKT/mTOR pathway via Cx43.
  • Establishes Cx43 as a critical link between natural compounds and oncogenic pathways in GC.
  • Highlights the non-channel scaffolding function of Cx43 as a therapeutic target for GC.
Keywords:
Cx43DioscinEMTGastric cancerVEGFA/PI3K/aKT/mTOR signaling pathway

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