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Dioscin augments HSV-tk-mediated suicide gene therapy for melanoma by promoting connexin-based intercellular

Jianyong Xiao1, Guangxian Zhang1, Bin Li2

  • 1Department of Biochemistry, Guangzhou University of Chinese Medicine, Guangzhou 510006, China.

Oncotarget
|December 2, 2016
PubMed

Insights

Dioscin enhances melanoma suicide gene therapy by boosting gap junction communication. This increases the bystander effect of herpes simplex virus thymidine kinase/ganciclovir (HSV-tk/GCV), leading to reduced tumor growth in preclinical models.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biotechnology

Background:

  • Suicide gene therapy offers promise for melanoma treatment but faces efficiency limitations due to gene transfer challenges.
  • Connexins (Cx26 and Cx43) are key components of gap junctions, facilitating intercellular communication.
  • Dioscin, a natural glucoside saponin, has shown potential in modulating cellular processes.

Purpose of the Study:

  • To investigate if dioscin can enhance the bystander effect of herpes simplex virus thymidine kinase/ganciclovir (HSV-tk/GCV) suicide gene therapy in melanoma.
  • To determine the role of dioscin in upregulating connexin expression and gap junction formation.
  • To evaluate the efficacy of combining dioscin with HSV-tk/GCV therapy in a preclinical melanoma model.

Main Methods:

  • Assessed dioscin's effect on connexin Cx26 and Cx43 expression in B16 melanoma cells.
  • Measured gap junctional intercellular communication (GJIC) using B16 melanoma cells treated with dioscin.
  • Evaluated the bystander effect of HSV-tk/GCV therapy in B16tk cells with and without dioscin treatment.
  • Investigated the impact of dominant-negative Cx43 overexpression on GJIC and bystander effect.
  • Conducted in vivo studies using tumor-bearing mice treated with a combination of dioscin and GCV.

Main Results:

  • Dioscin treatment increased the expression of connexins Cx26 and Cx43 in B16 melanoma cells.
  • Dioscin significantly enhanced GJIC in B16 melanoma cells.
  • GCV-induced bystander killing was more efficient in dioscin-treated B16tk cells.
  • Overexpression of dominant-negative Cx43 diminished GJIC and weakened the HSV-tk/GCV bystander effect.
  • Combination therapy with dioscin and GCV in vivo resulted in significant reductions in tumor volume and weight compared to monotherapy.

Conclusions:

  • Dioscin augments the bystander effect of the HSV-tk/GCV suicide gene therapy system.
  • The enhancement is mediated by dioscin's ability to increase connexin-mediated gap junction coupling.
  • Dioscin represents a potential adjuvant therapy to improve the efficacy of melanoma suicide gene therapy.
Keywords:
bystander effectconnexindioscinmelanomasuicide gene

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