Galectin-3 leads to attenuation of apoptosis through Bax heterodimerization in human thyroid carcinoma cells
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Yosuke Harazono1, Dhong Hyo Kho1, Vitaly Balan2, Kosei Nakajima1, Tianpeng Zhang1, Victor Hogan1 and Avraham Raz1
1 Departments of Oncology and Pathology, School of Medicine, Wayne State University, and Karmanos Cancer Institute, Detroit, MI
2 Everon Biosciences, Buffalo, NY
Raz Avraham, email:
Keywords: Galectin-3 (Gal-3), Bax, doxorubicin (DXR), apoptosis, thyroid cancer
Received: August 13, 2014 Accepted: September 15, 2014 Published: September 16, 2014
Cancer cells survive escaping normal apoptosis and the blocks in apoptosis that keep cancer cells alive are promising candidates for targeted therapy. Galectin-3 (Gal-3) is, a member of the lectin family, which is involved in cell growth, adhesion, proliferation and apoptosis. It remains elusive to understand the role of Gal-3 on apoptosis in thyroid carcinoma cells. Here, we report that Gal-3 heterodimerizes Bax, mediated by the carbohydrate recognition domain (CRD) of Gal-3, leading to anti-apoptotic characteristic. Gal-3/Bax interaction was suppressed by an antagonist of Gal-3, in which in turn cells became sensitive to apoptosis. The data presented here highlight that Gal-3 is involved in the anti-apoptosis of thyroid carcinoma cells. Thus, it suggests that targeting Gal-3 may lead to an improved therapeutic modality for thyroid cancer.
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