However, downregulation of Gelectin-3 inversely was also found in breast cancer, prostate cancer and endometrial cancer tissues,33–36 which might be due to changes in its cytosolic and nuclear expression pattern, activating distinct molecular mechanisms in different cancer types.37 In addition, Galectin-3 was generally considered as a cell adhesion molecule, but we found that Galectin-3 overexpression suppressed HCC cell adhesion whilst Galectin-3 suppression enhanced cell adhesion in this study. This evidence concerns the gene LGALS3 and cancer.