Dong Tang
Clinical Medical College of Yangzhou University, China
Title: High expression of galectin-1 in pancreatic stellate cells increases the progression of pancreatic cancer
Biography
Biography: Dong Tang
Abstract
Pancreatic cancer is one of the most common malignant tumors with poor prognosis due to extremely high malignancy, low rate of eligibility for surgical resection and chemoradiation resistance. Increasing evidence indicate that the interaction between activated pancreatic stellate cells (PSCs) and PDAC cells plays an important role in the development of PDAC. By producing high levels of cytokines, chemotactic factors, growth factors and excessive extracellular matrix (ECM), PSCs create desmoplasia and a hypoxic microenvironment that promote the initiation, development, evasion of immune surveillance, invasion, metastasis and resistance to chemoradiation of PDAC. Our founding suggested that 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 short survival. High expression in PSCs contributes to immune privilege in the pancreatic cancer microenvironment by enhancing apoptosis and anergy of T cells and skewing the Th1/Th2 cytokine balance. Further more, TGF-β1 from pancreatic cancer cells upregulated Galectin-1 expression in PSCs, and in turn to promotes the proliferative activity, MMP2 and MMP9 expression, and invasion of pancreatic cancer cells, as well as the tumor establishment, growth, and liver metastasis. High expression of Galectin-1 in pancreatic stellate cells may provides a therapeutic target for the treatment of pancreatic cancer.