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- W2950143268 abstract "Gap-junction-mediated cell-cell communication enables tumor cells to synchronize complex processes. We previously found that glioblastoma cancer stem cells (CSCs) express higher levels of the gap junction protein Cx46 compared to non-stem tumor cells (non-CSCs) and that this was necessary and sufficient for CSC maintenance. To understand the mechanism underlying this requirement, we use point mutants to disrupt specific functions of Cx46 and find that Cx46-mediated gap-junction coupling is critical for CSCs. To develop a Cx46 targeting strategy, we screen a clinically relevant small molecule library and identify clofazimine as an inhibitor of Cx46-specific cell-cell communication. Clofazimine attenuates proliferation, self-renewal, and tumor growth and synergizes with temozolomide to induce apoptosis. Although clofazimine does not cross the blood-brain barrier, the combination of clofazimine derivatives optimized for brain penetrance with standard-of-care therapies may target glioblastoma CSCs. Furthermore, these results demonstrate the importance of targeting cell-cell communication as an anti-cancer therapy." @default.
- W2950143268 created "2019-06-27" @default.
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- W2950143268 date "2019-04-01" @default.
- W2950143268 modified "2023-10-17" @default.
- W2950143268 title "Development of a Cx46 Targeting Strategy for Cancer Stem Cells" @default.
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- W2950143268 doi "https://doi.org/10.1016/j.celrep.2019.03.079" @default.
- W2950143268 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6497083" @default.
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