Figure 1.
Immunohistochemical analysis revealed that galectin-3 was located in the cytoplasm and membrane of breast cancer cells (A). Galectin-3 protein is expressed at a significantly higher level in breast cancer tissues compared to paracancerous tissue (B).
Table 1.
Galectin-3 expression and clinicopathological features (n = 1187).
Table 2.
Multivariate analysis of the factors related to post-operative distant metastasis.
Table 3.
Correlations between Galectin-3 expression and chemotherapeutic resistance in breast cancers (n = 135).
Figure 2.
ATO treatment (2.5 µM) induces limited apoptosis in breast cancer cells.
Untreated cells (top panel) and cells treated with ATO (bottom panel) were then analyzed by staining with PI and annexin V, followed by flow cytometry. The proportion of cells in apoptosis is shown in the figure.
Figure 3.
ATO treatment (2.5 µM) significantly increased endogenous galectin-3 expression in MDA-MB-231 cells.
Cells were treated with ATO and anti-galectin-3 antibody (1∶1000) was used to detect endogenous galectin-3 proteins. GAPDH was used as loading control. The results shown are the mean of at least 3 independent experiments. *P<0.01.
Figure 4.
The protein level of galectin-3 was reduced after shRNA treatment.
Three independent shRNAs against galectin-3 were used to construct stable cell lines.
Figure 5.
Galectin-3 knockdown sensitized MDA-MB-231 cells to ATO-induced apoptosis.
Cells were labeled with annexin V (x-axis) and PI (y-axis), and apoptosis was analyzed using a flow cytometer.
Figure 6.
Cell viability was reduced by combined galectin-3 knockdown and ATO treatment.