Research Papers:

Galectin-3 leads to attenuation of apoptosis through Bax heterodimerization in human thyroid carcinoma cells

Yosuke Harazono, Dhong Hyo Kho, Vitaly Balan, Kosei Nakajima, Tianpeng Zhang, Victor Hogan and Avraham Raz _

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Oncotarget. 2014; 5:9992-10001. https://doi.org/10.18632/oncotarget.2486

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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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