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

Oncotarget. 2014 Oct 30;5(20):9992-10001. doi: 10.18632/oncotarget.2486.

Abstract

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.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Apoptosis / physiology
  • Cell Line, Tumor
  • Cell Proliferation / physiology
  • Galectin 3 / metabolism*
  • Humans
  • Protein Multimerization
  • Thyroid Neoplasms / genetics
  • Thyroid Neoplasms / metabolism*
  • Thyroid Neoplasms / pathology*
  • bcl-2-Associated X Protein / metabolism*

Substances

  • BAX protein, human
  • Galectin 3
  • bcl-2-Associated X Protein