Inhibition of gap junctions sensitizes primary glioblastoma cells for temozolomide

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

Angaben zum Objekt

• Standort: Deutsche Nationalbibliothek Frankfurt am Main
• Umfang: Online-Ressource
• Sprache: Englisch
• Anmerkungen: issn: 2072-6694

Klassifikation und Themen

• Schlagwort: Glioblastom ; Gap junction ; Zelltod ; Jun

Beteiligte, Orts- und Zeitangaben

• Ereignis: Veröffentlichung
• (wo): Freiburg
• (wer): Universität
• (wann): 2019
• Urheber: Potthoff, Anna-Laura ; Heiland, Dieter Henrik ; Evert, Bernd O. ; Almeida, Filipe Rodrigues ; Behringer, Simon P. ; Dolf, Andreas ; Güresir, Agi ; Güresir, Erdem Özer ; Joseph, Kevin ; Pietsch, Torsten ; Schuß, Patrick ; Herrlinger, Ulrich ; Westhoff, Mike-Andrew ; Vatter, Hartmut ; Waha, Andreas ; Schneider, Matthias

Weitere Informationen

• DOI: 10.3390/cancers11060858
• URN: urn:nbn:de:bsz:25-freidok-1501319
• Rechteinformation: Der Zugriff auf das Objekt ist unbeschränkt möglich.
• Letzte Aktualisierung: 15.08.2025, 07:27 MESZ