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Pancreatic cancer is one of the most aggressive malignancies, with a 5-year overall survival of less than 5%. Tumor drug resistance to conventional chemotherapy, such as Gemcitabine, is often a significant contributor to poor overall survival. One of the common mechanisms of Gemcitabine resistance is activation of cell signaling via increased phosphorylation of mitogen-Activated kinase (MAP) kinases, leading to increased tumor survival and reduced sensitivity to chemotherapeutic agents. A growing body of evidence suggests that the CXCL12/CXCR4 signal transduction axis in the tumor microenvironment is an important mediator of tumor migration, growth, and drug resistance. We hypothesized that stromal cells such as carcinoma-associated fibroblasts (CAFs), an important cellular component of the tumor microenvironment (TME), play a contributory role in the growth, invasiveness, and drug response of pancreatic cancer cells (PCCs)

Stromal Carcinoma Associated Fibroblasts Promote Drug Resistance of Human Pancreatic Cancer Cells by Modulation of ROS via CXCR4/CXCL12 Signaling