Abstract

BACKGROUND: Galectin-1, a member of carbohydrate-binding proteins with apolyvalent function on tumor progression, was found strongly expressed inpancreatic satellite cells (PSCs), which partner in crime with cancer cells andpromote the development of pancreatic ductal adenocarcinoma (PDAC). Weevaluated the effects of PSCs derived Galectin-1 on the progression of PDAC, aswell as the tumor establishment and development in mouse xenografts.

METHODS:The relationship between immunohistochemistrystaining intensity of Galectin-1 and clinicopathologic variables were assessedin 66 PDAC tissues, 18 chronic pancreatitis tissues and 10 normal controls. Theroles of PSCs isolated from PDAC and normal pancreas on the proliferativeactivity, MMP2 and MMP9 expression, and the invasion of CFPAC-1 in theco-cultured system, as well as on the tumor establishment and development inmouse xenografts by mixed implanting with CFPAC-1 subcutaneously wereevaluated.

RESULTS:Galectin-1 expression was gradually increased fromnormal pancreas (negative), chronic pancreatitis (weak) to PDAC (strong), inwhich Galectin-1 expression was also increased from well, moderately to poorlydifferentiated PDAC. Galectin-1 staining intensity of pancreatic cancer tissuewas associated with increase in tumor size, lymph node metastasis, perineuralinvasion and differentiation and UICC stage, and served as the independentprognostic indicator of poor survival of pancreatic cancer. In vitro and invivo experiments indicated that TGF-β1 upregulated Galectin-1 expression inPSCs, which could further promotes the proliferative activity, MMP2 and MMP9expression, and invasion of pancreatic cancer cells, as well as the tumorestablishment and growth.

CONCLUSION:Galectin-1 expression in stromal cells ofpancreatic cancer suggests that this protein plays a role in the promotion ofcancer cells invasion and metastasis and provides a therapeutic target for thetreatment of pancreatic cancer.