Abstract
BackgroundGalectin-1, a member of carbohydrate-binding proteins with a polyvalent function on tumor progression, was found strongly expressed in pancreatic satellite cells (PSCs), which partner in crime with cancer cells and promote the development of pancreatic ductal adenocarcinoma (PDAC). We evaluated the effects of PSCs derived Galectin-1 on the progression of PDAC, as well as the tumor establishment and development in mouse xenografts.MethodsThe relationship between immunohistochemistry staining intensity of Galectin-1 and clinicopathologic variables were assessed in 66 PDAC tissues, 18 chronic pancreatitis tissues and 10 normal controls. The roles of PSCs isolated from PDAC and normal pancreas on the proliferative activity, MMP2 and MMP9 expression, and the invasion of CFPAC-1 in the co-cultured system, as well as on the tumor establishment and development in mouse xenografts by mixed implanting with CFPAC-1 subcutaneously were evaluated.ResultsGalectin-1 expression was gradually increased from normal pancreas (negative), chronic pancreatitis (weak) to PDAC (strong), in which Galectin-1 expression was also increased from well, moderately to poorly differentiated PDAC. Galectin-1 staining intensity of pancreatic cancer tissue was associated with increase in tumor size, lymph node metastasis, perineural invasion and differentiation and UICC stage, and served as the independent prognostic indicator of poor survival of pancreatic cancer. In vitro and in vivo experiments indicated that TGF-β1 upregulated Galectin-1 expression in PSCs, which could further promotes the proliferative activity, MMP2 and MMP9 expression, and invasion of pancreatic cancer cells, as well as the tumor establishment and growth.ConclusionGalectin-1 expression in stromal cells of pancreatic cancer suggests that this protein plays a role in the promotion of cancer cells invasion and metastasis and provides a therapeutic target for the treatment of pancreatic cancer.
Highlights
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal human malignancies with occult onset and poor prognosis[1]
The results indicated that the expression of Galectin-1 increased gradually from normal pancreas, chronic pancreatitis to pancreatic ductal adenocarcinoma (PDAC) (Table 1, Figure 1)
Galectin-1 was negative in normal pancreas, whereas weak or moderate staining was mainly observed in the mesenchymal of chronic pancreatitis tissues (Figure 1 a,b)
Summary
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal human malignancies with occult onset and poor prognosis[1]. Sufficient knowledge of the cellular function coupled to the distinctive anatomical features of pancreatic cancer would give hope for developing new methods of early detection, screening and diagnostic, as well as the treatment opportunities. Hithreto, increasing evidences had showed that pancreatic satellite cells (PSCs), a main source of the stromal of pancreatic cancer, partnered in crime with cancer cells and promoted the development of pancreatic cancer [6,7]. Galectin-1, a member of carbohydrate-binding proteins with a polyvalent function on tumor progression, was found strongly expressed in pancreatic satellite cells (PSCs), which partner in crime with cancer cells and promote the development of pancreatic ductal adenocarcinoma (PDAC). We evaluated the effects of PSCs derived Galectin-1 on the progression of PDAC, as well as the tumor establishment and development in mouse xenografts
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