Cx26 drives self-renewal in triple-negative breast cancer via interaction with NANOG and focal adhesion kinase.

ABSTRACT: Tumors adapt their phenotypes during growth and in response to therapies through dynamic changes in cellular processes. Connexin proteins enable such dynamic changes during development, and their dysregulation leads to disease states. The gap junction communication channels formed by connexins have been reported to exhibit tumor-suppressive functions, including in triple-negative breast cancer (TNBC). However, we find that connexin 26 (Cx26) is elevated in self-renewing cancer stem cells (CSCs) and is necessary and sufficient for their maintenance. Cx26 promotes CSC self-renewal by forming a signaling complex with the pluripotency transcription factor NANOG and focal adhesion kinase (FAK), resulting in NANOG stabilization and FAK activation. This FAK/NANOG-containing complex is not formed

SUBMITTER: Thiagarajan PS 

PROVIDER: S-EPMC5805730 | biostudies-literature | 2018 Feb

REPOSITORIES: biostudies-literature