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- W2950581103 abstract "Gap junctions have recently been shown to interconnect glioblastoma cells to a multicellular syncytial network, thereby allowing intercellular communication over long distances as well as enabling glioblastoma cells to form routes for brain microinvasion. Against this backdrop gap junction-targeted therapies might provide for an essential contribution to isolate cancer cells within the brain, thus increasing the tumor cells’ vulnerability to the standard chemotherapeutic agent temozolomide. By utilizing INI-0602—a novel gap junction inhibitor optimized for crossing the blood brain barrier—in an oncological setting, the present study was aimed at evaluating the potential of gap junction-targeted therapy on primary human glioblastoma cell populations. Pharmacological inhibition of gap junctions profoundly sensitized primary glioblastoma cells to temozolomide-mediated cell death. On the molecular level, gap junction inhibition was associated with elevated activity of the JNK signaling pathway. With the use of a novel gap junction inhibitor capable of crossing the blood–brain barrier—thus constituting an auspicious drug for clinical applicability—these results may constitute a promising new therapeutic strategy in the field of current translational glioblastoma research." @default.
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- W2950581103 date "2019-06-20" @default.
- W2950581103 modified "2023-10-17" @default.
- W2950581103 title "Inhibition of Gap Junctions Sensitizes Primary Glioblastoma Cells for Temozolomide" @default.
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- W2950581103 doi "https://doi.org/10.3390/cancers11060858" @default.
- W2950581103 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6628126" @default.
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