Galectin-3: A factotum in carcinogenesis bestowing an archery for prevention

T Jeethy Ram1,2, Asha Lekshmi1, Thara Somanathan3

  • 1Division of Cancer Research, Regional Cancer Centre, Medical College, Trivandrum, Kerala, India.

Insights

Galectin-3 (gal-3) drives cancer metastasis and therapy resistance by aiding tumor cell survival and spread. Inhibiting gal-3 offers a promising strategy to prevent cancer progression and enhance treatment efficacy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Glycobiology

Background:

  • Cancer metastasis and therapy resistance are critical challenges in oncology.
  • Galectins are a family of carbohydrate-binding proteins involved in various cellular processes.
  • Galectin-3 (gal-3) is a unique multifaceted glycosylated molecule with diverse intracellular and extracellular functions.

Purpose of the Study:

  • To review the functional aspects of galectin-3 (gal-3).
  • To elucidate the role of gal-3 in cancer metastasis and therapy resistance.
  • To explore the potential of gal-3 inhibitors as a therapeutic strategy.

Main Methods:

  • Literature review of studies on galectin-3.
  • Searches conducted in PubMed, Scopus, and Google Scholar.
  • Analysis of gal-3's involvement in cellular differentiation, transformation, and metastasis.

Main Results:

  • Galectin-3 (gal-3) is crucial in tumor metastasis, promoting cancer cell survival in circulation and extravasation.
  • Gal-3 plays a role in immune surveillance, angiogenesis, and establishing therapy resistance, particularly via epithelial-mesenchymal transition.
  • Gal-3 deregulation is linked to cancer progression and metastasis.

Conclusions:

  • Targeting galectin-3 (gal-3) through inhibitors presents an innovative strategy for cancer prevention and overcoming therapeutic resistance.
  • Further systematic studies on glycosylation and gal-3 antagonists are warranted for clinical applications.
  • Inhibiting gal-3 activity could be a key to blocking cancer progression and metastasis.

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