FOXC1-induced Gli2 activation: A non-canonical pathway contributing to stemness and anti-Hedgehog resistance in basal-like breast cancer

Bingchen Han; Ying Qu; Yi Yu-Rice; Jeffrey Johnson; Xiaojiang Cui

doi:10.1080/23723556.2015.1131668

FOXC1-induced Gli2 activation: A non-canonical pathway contributing to stemness and anti-Hedgehog resistance in basal-like breast cancer

Mol Cell Oncol. 2016 Jan 11;3(3):e1131668. doi: 10.1080/23723556.2015.1131668. eCollection 2016 May.

Authors

Bingchen Han¹, Ying Qu¹, Yi Yu-Rice¹, Jeffrey Johnson¹, Xiaojiang Cui¹

Affiliation

¹ Department of Surgery, Samuel Oschin Cancer Institute, Cedars-Sinai Medical Center , Los Angeles, CA, USA.

Abstract

The Forkhead box C1 (FOXC1) transcriptional factor is a critical biomarker for basal-like breast cancer (BLBC). We recently reported that FOXC1 promotes cancer stem cell properties in BLBC by activating Smoothened (SMO)-independent Hedgehog (Hh) signaling, suggesting a FOXC1-mediated mechanism for BLBC cell function and anti-Hh therapy resistance.

Keywords: Basal-like breast cancer; FOXC1; GLI2; Hedgehog; Smoothened; cancer stem cells.

Grants and funding

R01 CA151610/CA/NCI NIH HHS/United States