Galectin-1, a β-galactoside-
binding protein implicated in
cancer cell immune privilege, was highly expressed in activated pancreatic stellate cells (PSCs). This study was designed to investigate the relationship between PSC-derived
galectin-1 and
tumor immunity in
pancreatic cancer. Isolated PSCs were identified as normal pancreas cells (hNPSCs) or
pancreatic cancer cells (hCaPSCs) by immunohistochemical staining for α-SMA and
vimentin, and
galectin-1 expression was evaluated by Western blotting and quantitative RT-PCR. Apoptosis,
caspase activity, and
cytokine production (IL-6, IL-10, TNF-β, and IFN-γ) of T cells co-cultured with PSCs were evaluated, and immunohistochemical staining of
galectin-1 was correlated with CD3 and clinicopathological variables in 66
pancreatic cancer and 10 normal pancreatic tissue samples. hCaPSCs exhibited higher
galectin-1 expression than did hNPSCs, and hCaPSCs induced higher levels of apoptosis in T cells following co-culture. hCaPSCs activated
caspase-9 and
caspase-3 in the mitochondrial apoptotic pathway and stimulated secretion of Th2
cytokines (IL-6 and IL-10) but decreased secretion of Th1
cytokines (TNF-β and IFN-γ), compared with hNPSCs. Immunohistochemical staining indicated that
galectin-1 and CD3 were more highly expressed in
pancreatic cancer tissue.
Galectin-1 expression was highest in poorly differentiated
pancreatic cancer cells and lowest in well-differentiated
pancreatic cancer cells and was associated with
tumor size,
lymph node metastasis, differentiation, and UICC stage. However, CD3 expression showed the opposite trend and was highest in well-differentiated
pancreatic cancer cells and was associated with
tumor differentiation and UICC stage. High expression of
galectin-1 was associated with short survival, as was low expression of CD3. hCaPSC-derived
galectin-1 enhanced apoptosis and anergy of T cells in
pancreatic cancer, which contributes to the immune escape of
pancreatic cancer cells.