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A Rapid Screening Workflow to Identify Potential Combination Therapy for GBM using Patient-Derived Glioma Stem Cells
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Novel approach to temozolomide resistance in malignant glioma: connexin43-directed therapeutics

Christina L Grek1, Zhi Sheng2, Christian C Naus3

  • 1FirstString Research, Inc., Mount Pleasant, SC, USA.

Current Opinion in Pharmacology
|May 28, 2018
PubMed

Insights

Connexin43 (Cx43) protein contributes to glioblastoma (GBM) resistance to temozolomide (TMZ) chemotherapy. Cx43 peptidomimetics offer a promising therapeutic strategy to overcome this resistance, potentially through modulating tumor microenvironment interactions.

Area of Science:

  • Neuro-oncology
  • Molecular biology
  • Cancer therapeutics

Background:

  • Malignant glioma, particularly glioblastoma (GBM), exhibits significant resistance to temozolomide (TMZ) chemotherapy.
  • The gap junction protein connexin43 (Cx43) plays a multifaceted role in glioma development and progression.
  • Cx43 is implicated in conferring chemotherapeutic resistance to GBM cells and influencing the tumor microenvironment.

Purpose of the Study:

  • To review recent advancements in understanding the role of Cx43 in malignant glioma.
  • To highlight Cx43's involvement in the tumor microenvironment and TMZ resistance.
  • To explore the therapeutic potential of Cx43 peptidomimetics in overcoming TMZ resistance.

Main Methods:

  • Literature review focusing on Cx43, malignant glioma, tumor microenvironment, and temozolomide resistance.
  • Analysis of studies investigating Cx43 peptidomimetics as a therapeutic strategy.
  • Discussion of in vitro models and patient-derived stem cells for personalized drug screening.

Main Results:

  • Cx43 contributes to TMZ resistance in GBM, potentially by influencing cell-cell communication and signaling pathways.
  • Cx43 peptidomimetics demonstrate therapeutic promise in preclinical models of TMZ-resistant glioma.
  • Tumor heterogeneity presents challenges for targeted Cx43 therapies, emphasizing the need for advanced in vitro models.

Conclusions:

  • Cx43 is a critical factor in malignant glioma's resistance to TMZ.
  • Cx43 peptidomimetics represent a viable therapeutic avenue for overcoming TMZ resistance.
  • Developing patient-specific in vitro models is crucial for advancing Cx43-targeted therapies and personalized treatment strategies.

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