Relationship between galectin-3 expression and TRAIL sensitivity in breast cancer

Abstract

Evaluation of: Mazurek N, Byrd JC, Sun Y, Ueno S, Bresalier RS. A galectin-3 sequence polymorphism confers TRAIL sensitivity to human breast cancer cells. Cancer DOI: 10.1002/cncr.26078 (2011) (Epub ahead of print).

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) binds to death receptors expressed on cancer cells and induces apoptosis. Triple-negative breast cancer cell lines are more sensitive to TRAIL or TRAIL-death receptor agonistic monoclonal antibody-induced apoptosis compared with HER-2/neu-overexpressing or luminal cell lines. The paper under evaluation sought to determine whether the His64/Pro64 polymorphism of galectin-3, which is associated with breast cancer incidence, affects sensitivity to TRAIL. None of five breast cancer cell lines homozygous for Pro64 galectin-3 were sensitive to TRAIL, but two out of two homozygous His64 cell lines and one out of two heterozygous His64 cell lines were sensitive. Transfection of galectin-3 null BT549 breast cancer cells with His64 galectin-3 rendered them sensitive to TRAIL, while Pro64 galectin-3-transfected cells remained resistant to TRAIL. This article highlights that galectin-3 receptor expression and genotype may be useful markers in predicting TRAIL or agonistic antibody sensitivity of breast cancer patients.

Keywords::

• breast cancer
• galectin-3
• triple-negative breast cancer
• tumor necrosis factor-related apoptosis-inducing ligand

Financial & competing interests disclosure

Donald J Buchsbaum has intellectual property interests related to the TRA-8 anti-DR5 antibody licensed by the University of Alabama at Birmingham to Daiichi Sankyo (Tokyo, Japan). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.