Journal
CANCER CELL
Volume 35, Issue 1, Pages 64-+Publisher
CELL PRESS
DOI: 10.1016/j.ccell.2018.11.016
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Funding
- Brewster Foundation
- US Department of Defense [BC123187]
- Susan G. Komen [PDF17332118]
- NJCCR [DFHS15PPCO21]
- Pre-clinical Imaging and Flow Cytometry Shared Resources of the Rutgers Cancer Institute of New Jersey [P30CA072720]
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Triple-negative breast cancer (TNBC) patients have the worst prognosis and distant metastasis-free survival among all major subtypes of breast cancer. The poor clinical outlook is further exacerbated by a lack of effective targeted therapies for TNBC. Here we show that ectopic expression and therapeutic delivery of the secreted protein Tubulointerstitial nephritis antigen-like 1 (Tinagl1) suppresses TNBC progression and metastasis through direct binding to integrin alpha 5 beta 1, alpha v beta 1, and epidermal growth factor receptor (EGFR), and subsequent simultaneous inhibition of focal adhesion kinase (FAK) and EGFR signaling pathways. Moreover, Tinagl1 protein level is associated with good prognosis and reversely correlates with FAK and EGFR activation status in TNBC. Our results suggest Tinagl1 as a candidate therapeutic agent for TNBC by dual inhibition of integrin/FAK and EGFR signaling pathways.
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