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Functions of pancreatic stellate cell-derived soluble factors in the microenvironment of pancreatic ductal carcinoma
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Abstract
Qi Wu1,*, Ying Tian1,*, Jingqiu Zhang2,*, Hongpeng Zhang1, Fengming Gu1, Yongdie Lu1, Shengnan Zou1, Yuji Chen1, Pengxiang Sun1, Mengyue Xu1, Xiaoming Sun1, Chao Xia3, Hao Chi1, A Ying Zhu1, Dong Tang2 and Daorong Wang2
1Medical College of Yangzhou University, Yangzhou, P.R. China
2Department of General Surgery, Institute of General Surgery, Northern Jiangsu Province Hospital, Clinical Medical College, Yangzhou University, Yangzhou, P.R. China
3Nanjing Medical University, Nanjing, P.R. China
*These authors contributed equally to this work
Correspondence to:
Dong Tang, email: [email protected]
Daorong Wang, email: [email protected]
Keywords: transforming growth factor β(TGF-β), interleukin 6(IL-6), galectin-1, stromal cell-derived factor-1(SDF-1), hepatocyte growth factor (HGF)
Received: July 26, 2017 Accepted: September 21, 2017 Published: October 19, 2017
ABSTRACT
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal forms of cancer with poor prognosis because it is highly resistant to traditional chemotherapy and radiotherapy and it has a low rate of surgical resection eligibility. Pancreatic stellate cells (PSC) have become a research hotspot in recent years, and play a vital role in PDAC microenvironment by secreting soluble factors such as transforming growth factor β, interleukin-6, stromal cell-derived factor-1, hepatocyte growth factor and galectin-1. These PSC-derived cytokines and proteins contribute to PSC activation, participating in PDAC cell proliferation, migration, fibrosis, angiogenesis, immunosuppression, epithelial–mesenchymal transition, and chemoradiation resistance, leading to malignant outcome. Consequently, targeting these cytokines and proteins or their downstream signaling pathways is promising for treating PDAC.
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