Unlike other members of the galectin family the functional role of Galectin-12 (Gal-12) in carcinogenesis is largely unexplored. However, evidence is accumulating suggesting it as an important modulator in controlling tumor growth and progression.We have previously shown that Gal-12 expression is lost in colon cancer due to epigenetic silencing. In order to decipher the biological consequence of re-expression of Gal-12 on colon cancer tumorigenesis we established a colon cancer model cell line which facilitates inducible expression of Gal-12 at physiological levels. Analyzing its subcellular localization revealed colocalization with splicing speckles suggesting Gal-12 as a potent modulator of pre-mRNA splicing and processing.
Currently we are applying different approaches to investigate the impact of Gal-12 on maintaining cellular homeostasis at a molecular level in detail. Our vision is to decipher to what extent this protein interferes with tumor growth which could be particularly relevant for the development of novel strategies to inhibit colon cancer growth.