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Updated: Apr 21, 2026

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

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

Yosuke Harazono1, Dhong Hyo Kho1, Vitaly Balan2

  • 1Departments of Oncology and Pathology, School of Medicine, Wayne State University, and Karmanos Cancer Institute, Detroit, MI.

Oncotarget
|November 14, 2014
PubMed

Insights

Targeting cancer cell survival, this study reveals Galectin-3 (Gal-3) promotes thyroid cancer cell anti-apoptosis by interacting with Bax. Inhibiting Gal-3 restores apoptosis, suggesting it as a therapeutic target for thyroid cancer.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • Cancer cells evade apoptosis, a key mechanism for survival and therapeutic resistance.
  • Galectin-3 (Gal-3), a lectin, influences cell processes including apoptosis, but its role in thyroid carcinoma is unclear.

Purpose of the Study:

  • To elucidate the role of Galectin-3 (Gal-3) in regulating apoptosis within thyroid carcinoma cells.
  • To investigate the molecular mechanism by which Gal-3 affects apoptosis in thyroid cancer.

Main Methods:

  • Investigated Gal-3 interaction with Bax using biochemical assays.
  • Utilized a Gal-3 antagonist to assess its impact on apoptosis sensitivity.
  • Examined the role of Gal-3's carbohydrate recognition domain (CRD) in mediating interactions.

Main Results:

  • Galectin-3 (Gal-3) forms heterodimers with Bax, mediated by its CRD, conferring anti-apoptotic properties.
  • Suppression of Gal-3/Bax interaction using a Gal-3 antagonist sensitized thyroid carcinoma cells to apoptosis.
  • Confirmed Gal-3's involvement in promoting the survival of thyroid carcinoma cells.

Conclusions:

  • Galectin-3 (Gal-3) plays a significant role in the anti-apoptotic mechanisms of thyroid carcinoma.
  • Targeting Galectin-3 presents a potential therapeutic strategy for enhancing apoptosis and treating thyroid cancer.

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